Melanoma can be treated by interleukin-9 protein

US researchers found through research involving recombinant dog proteins that a protein has the efficacy of treating the skin cancer melanoma. This protein can be synthesized by the human body, so it is expected to develop new treatment to promote the body to fight against melanoma on this basis.

Melanoma is a malignant skin cancer, and the mortality rate is high. The researchers from Harvard University School of Medicine and other institutions conducted research on some melanoma patients with tissue samples and found that compared with normal levels, the patient code number for the interleukin-9 protein content is much lower or even missing.

The researchers also explored the effect of this protein on melanoma through animal experiments, and the results showed that if the mice injected with the inhibitory effect of interleukin-9 substances, the melanoma they suffer will grow rapidly, which is similar to human patients who have this protein in vivo.

However, if mice were injected with substances that promote an increase in their interleukin-9 levels, the rate at which they develop melanoma will decrease. This suggests that interleukin-9 is a protein that inhibits melanoma.

Interleukin-9 can achieve self-synthesis in the human and experimental mice, and we knew that it is a signal molecule which can mobilize the immune system in the past. The researchers suggested that in the future treatment of melanoma patients, it is suggested to promote the synthesis of more human interleukin-9 to mobilize the power of the immune system itself to inhibit tumor growth. Cusabio provides you with high-quality recombinant proteins such as recombinant Nrg2 at good prices.

This protein may be harmful for the body to remove HIV

A team of researchers led by UCLA found through research using recombinant human proteins that blocking a key protein which plays an important role in initiating an antiviral immune response may actually help to fight AIDS.

A result from animal studies suggests that for people with chronic infection with HIV, temporarily blocking a class of proteins called type I interferons can restore immune function and accelerate the antiviral effect of antiviral drugs. This is the first study to show that type I interferons play a role in HIV infection, i.e. the type I interferon can drive the body's immune destruction.

"This finding is completely counterintuitive, because many people believe that the more interferon, the better the anti-viral effect," members from UCLA AIDS Research Institute said, "Our research shows that in the chronic phase of HIV infection, interferon has a negative impact on the body to fight HIV and other types of infection or cancer. In fact, it may accelerate AIDS."

The idea is to reduce the chronic activation of immune cells by blocking type I interferons, allowing the tired CD8 T cells to have time to restore their ability and combat effectiveness. Combined with antiretroviral therapy, both can restore the body's immune function but also eradicate the HIV virus. The researchers used a "humanized mouse" whose immune system was replaced by the body's immune system cells, thymus tissue, and bone marrow. They used HIV-infected mouse antibodies to block type I interferons, which allowed the immune system to recover from the exhausted state, allowing the immune system to produce enough CD8 T cells to prepare for attack and kill HIV-infected cells. When combined with antiretroviral therapy, the therapy accelerates antiretroviral therapy to suppress HIV.

"We found that the results were contrary to our own intuition, which reduced the amount of virus and had a beneficial effect on improving the immune response to the virus."

But researchers say more experiments are needed before nonhuman primates conduct clinical trials in humans to determine whether the researchers' theory is valid and whether the therapy is safe in humans. Flarebio provides superior recombinant proteins including recombinant COLEC12 at competitive prices.

Piezo2 is clearly an important part of the respiratory process

A team of members of several US research institutions has found evidence that a protein has some control over the respiration process in mice through recombinant horse proteins. In their paper published in the journal Nature, the team described their study of protein Piezo2 and its multifaceted effects on regulating respiration. In France, Christo Goridis and the French Institute for Biological Products provided a report on the team's work in the same issue, outlining what the team was looking for and how they experimented and what they found.

As Goridis points out, previous studies have shown that many animals including humans have so-called Hering-Breuer reflections. This is an automatic mechanism that stops breathing when the lungs are filled and prevents damage caused by overfilling. But so far, little is known about the mechanisms involved in this process. To learn more, the team began by observing the vagal sensory neurons in the airway of mice, and previous studies have shown its role in breathing - they convey information about the condition of the lungs to the brain. Previous studies have also shown that the Piezo2 protein does participate in the process, although it is unclear how it works. In this new effort, researchers have learned more about protein expression in the lung system and their role.

The team examined all parts of the mice that were involved in respiration, which showed Piezo2 expression in nodular and jugular ganglia, some spinal sensory neurons and lung tissues. In order to find out the role of the protein in different regions, the team disabled the gene responsible for the expression of the protein. They found that the absence of Piezo2 in the jugular and dorsal root neurons resulted in neonatal death from respiratory distress. The production of proteins in nodular neurons shut down mice to adulthood but prevented the activation of Hering-Breuer reflexes - mice that inhale an unusual amount of air during normal respiration. The researchers also designed some of the light involved in the neural response, allowing the activation and inactivation of Piezo2 expression. This allowed the researchers to cause Hering-Breuer reflections only by turning on the light.

The researchers summed up their findings that Piezo2 is clearly an important part of the respiratory process. They noted that more work needs to be done to get a clearer picture of how the entire respiration process works. By the way, Flarebio provides you with superior recombinant proteins including recombinant ITGB2 for your research.

New method of anti-cancer method: taking advantage of drug resistance of cancer cells

Due to the resistance of cancer cells, the function of proteasome inhibitors in the treatment of cancer is limited. According to this study using recombinant mouse proteins, researchers at the Whitehead Institute have found a mechanism of resistance that occurs naturally in a variety of cancers that expose the fragility of drugs and stimulate natural cell death.

The finding, published in the Proceedings of the National Academy of Sciences, is titled "Inhibition of 19 s proteasome unit labeling of cell changes in various cancer states".

Hydrolases are large protein complexes that play an important role in regulating degradation and maintaining intracellular protein balance. When the cells become cancerous and produce tremendous pressure and are responsible for maintaining the protein balance. This goal is called proteasome inhibitors. Although proteasome inhibitors are effective in killing cancer cells in culture dishes (in vitro), they are severely limited in clinical use because of their resistance.

"At the moment, we have discovered an intuitive mechanism by which cells can obtain proteasome inhibitors in vitro," explains the team leader. "In our report, we describe in detail the effects of this mechanism on a variety of human cancers. In addition, we have determined that this mechanism is widely present in cells in a wide variety of states and can be combined with existing drugs."

By analyzing thousands of cancer cells and tumors, the researchers found that those cells resistant to proteasome inhibitors were inhibited.

In addition to resistance to proteasome inhibitors, the researchers report that inhibition of the expression of the proteasome subunit reflects a wide range of cellular genetic alterations. This facilitates treatment with biomarker methods.

"Resistance to cancer stems from multiple mechanisms, genetic or epigenetics. With this finding, we can develop new strategies and new compounds as arrays and make use of their drug-resistant properties which are more susceptible to effectively treat a variety of cancer types," said the research team leader. Flarebio provides you with high-quality recombinant proteins like recombinant ITGB2 at good prices.

The new target of gastric cancer has been found

Professor Zhang Hao of Shantou University and Nobel Laureate Professor Andrew Schally of Miami University have found found through recombinant human proteins that growth hormone receptor (GHRH-R) can be used as a new target in the treatment of gastric cancer. The research was published in the Proceedings of the National Academy of Sciences (PNAS) on December 7th.

Gastric cancer is the world's highest incidence of tumors in the top four, and it is one of the leading causes of death of cancer. There are nearly half of the world's new cases of gastric cancer in China. Clinical treatment for gastric cancer includes surgery, chemotherapy and radiotherapy. But the treatment effect is limited, and the recurrence rate can still be as high as about 40% forⅡ Ⅳ stage gastric cancer patients.

It is understood that gastric cancer is a heterogeneous malignant tumor, and to take personalized treatment program for different targets is the key to capture gastric cancer. At present, despite the molecular heterogeneity of gastric cancer has been carried out in terms of molecular typing; the data come from a limited population of gastric cancer patients. There is no clear and recognized molecular classification of gastric cancer, and related study has not played a role in clinical treatment.

Growth Hormone-Releasing Honnone (GHRH) is a classic endocrine hormone. Under physiological conditions, GHRH is secreted by human hypothalamus and plays a role in regulation of GHRH-R binding to pituitary cells. Recently, GHRH and GHRH-R pathways have also been found to be abnormally expressed in tumors.

Zhang Hao group found that GHRH-R levels in protein in samples, RNA and DNA in gastric cancer patients were abnormal. Abnormal expression of GHRH-R is closely related to the prognosis of cancer patients and can be used as an indicator of prognosis. The researchers used their own synthesis of the target GHRH-R of the polypeptide to carry out treatment studies and found that the targeting of the peptide can be effective to inhibit the tumor growth in vitro and in vivo.

The study showed that the peptide drug targeting GHRH-R blocked the activity of the key proteins of inflammatory carcinomas NFkB and STAT3 by reducing PAK1, a tumor node gene. This study provides important evidence for clinical trials of targeting GHRH-R drugs in the treatment of malignancies. Cusabio offers good-quality recombinant proteins such as recombinant PIGR at good prices.

The mechanisms by which cells are used to discover and remove organelles

Through research involving recombinant horse proteins, researchers at UT Southwestern Medical Center have discovered the mechanisms by which cells are used to discover and remove organelles. They are known as mitochondria. When these organelles are damaged, it can cause genetic problems such as cancer, neurodegenerative diseases, inflammatory diseases and aging. Dr. Beth Levine, director of the UT Southwestern Automation Research Center and Dr. Beth Levine, a senior author of the study, said in a recent presentation that understanding how the process works may lead to new treatments to prevent certain diseases and even certain aspects of aging. The Autophagy Research Center is the only autophagy research center in the country.

Because mitochondria are high in energy, when they are damaged, toxic chemicals that release reactive oxygen species are released to the rest of the cell. Removal of damaged mitochondria by autophagy, known as mitochondrial autophagy, is important for cellular health. Researchers have noted that the discovery of tag proteins on the mitochondrial outer membrane - specifically the Parkin- proteins attached to these tags - explains cell degrading organelles, called autophagosomes, and it targets to pathological mitochondria.

In the study, the researchers found a protein present on the mitochondrial membrane prohibitin 2 (PHB2), but PHB2 was exposed to the damaged mitochondrial outer membrane. Once the cells break, the protein LC3 in the autophagy outside the role of monitoring, and LC3 will be attracted to the PHB2 protein. The LC3 protein then attaches to PHB2, and the autophagosome carries the damaged organelle to the lysosome - another organelle found in the cell, acting like a tiny stomach with enzymes that break down cell waste.

"This study found that PHB2 is critical for targeted mitochondrial autophagic degradation," said Dr. Levine, "Previous studies have linked the presence of PHB2 to the prevention of cancer, aging, neurodegeneration, and inflammation. Significantly, the key role of PHB2 is to help to get rid of damaged mitochondria in cells, playing a catalytic role."

The study also found that PHB2 is necessary to routinely remove the maternally-derived mitochondrial DNA from the developing embryo, leaving only maternal DNA from the mother. This is a work done in roundworms, but there is a recent study conducted in mice using a mouse model elsewhere suggesting that mitochondria are also used to remove paternal mitochondria in mammalian embryos," said Dr. Wu Chung, a postdoctoral fellow at UT Southwestern, the first author of the study.

"Typically, only maternal mitochondrial DNA is passed on to offspring," Dr. Levine said. For unknown reasons, the presence of paternal mitochondrial DNA predicts some genetic or health problems in the offspring. In another finding, the UTSW study showed that PHB2 is essential for the Parkin effect, although scientists are paying more attention to Parkin's role in supporting autophagic PHB2. Flarebio offers superior recombinant proteins including recombinant Cd44 at good prices.

The supplementation of folic acid can reduce the risk of chronic kidney disease

Through research using recombinant human proteins, Professor Hou Fanfan and Professor Xu Xin at Southern Medical University recently published a study in the Journal of Internal Medicine to first confirm that adequate supplementation of folic acid can significantly slow down the process of renal disease in patients with hypertension and reduce the risk of chronic kidney disease developing to uremia. Folic acid is cheap and easy to take and very safe, and it is suitable for high-risk groups as a means of prevention and treatment.

Chronic kidney disease has become a public health problem affecting 120 million people in China. Uremic patients can only rely on life-long dialysis or renal transplantation to survive, consuming huge medical resources. Chronic kidney disease patients also have a high risk of concurrent stroke and other cardiovascular and cerebrovascular events. Therefore, how to effectively delay the progress of chronic kidney disease and to prevent cardiovascular and cerebrovascular events have been the medical profession and the medical and health sector focus.

The study recruited more than 15,000 adult hypertensive patients from China's 20 rural communities to participate in the Chinese stroke primary prevention trial with an average age of 60 years. Patients were randomized to depressurization plus folic acid supplementation (10 mg of enalapril per day and 10 mg of enalapril per day) with an average duration of treatment of 4.4 year. The results showed that supplementation with folic acid significantly reduced the rate of renal dysfunction in hypertensive patients and reduced the risk of developing renal disease by 21% compared with antihypertensive therapy alone. In 1,671 patients with CKD prior to treatment, supplementation with folic acid reduced the risk of developing kidney disease by 56% and significantly reduced the risk of rapid renal impairment and the development and mortality of kidney disease.

It is understood that the lack of folic acid is very common in China, the average serum level was significantly lower than the Western population, which may be related to eating habits and genetic. In view of the importance of folic acid to human health, the United States and Canada have begun to add in cereals such as flour folic acid since 1998. China has not yet implemented a supplementary public health policy of folic acid, folic acid deficiency may also be a common cause of our population.

Epidemiological studies conducted early in the study showed that folic acid deficiency is a risk factor for the development of renal disease in Chinese rural communities. In response to this feature, the team conducted the above-mentioned folic acid supplementation delayed renal dysfunction in a randomized controlled study. The study also confirmed that supplementation of folic acid can effectively reduce the risk of stroke in patients with primary hypertension. Flarebio offers good-quality recombinant proteins like recombinant TLR2 at competitive prices.

Aspirin indirectly inhibits the cancer proteins responsible for malignant cells

This study conducted by the University of Oregon Health Sciences (OHSU) and Oregon State University (OSU) was published in the AJP Cell Physiology Journal, which also publishes other studies on recombinant horse proteins. "The benefits of aspirin may be due to its effect on blood cells called platelets, rather than acting directly on tumor cells," said senior author Owen McCarty, a professor of OHSU's Department of Biomedical Engineering.

Platelets are tiny blood cells that help the body form clots to stop bleeding if necessary. It seems that platelets also increase the level of certain proteins that can support cancer cells and help them spread. This "oncoprotein" is referred to as c-MYC. The biological function of c-MYC is to regulate more than 15% of human gene expression. C-MYC regulators control cell life and death cycle, protein synthesis and cell metabolism. However, studies have shown that in cancer, the oncogene is overexpressed.

The researchers of the new study explain that aspirin reduces the ability of platelets to increase c-MYC oncoprotein levels. "Our work suggests that some of the anti-cancer effects of aspirin may be as follows: during blood transport, circulating tumor cells interact with platelets that stimulate tumor cells to survive by activating oncogenes such as c-MYC." Aspirin reduces platelet and tumor cell between the signals, thereby indirectly reducing the tumor cell growth.

Craig Williams, a professor at the OSU / OHSU School of Pharmacy and a co-author of the study, further explained this process. "Early cancer cells live in a very hostile environment where the immune system attacks regularly and tries to eliminate them," he said. "Platelets can protect and help to metastasize those early cancer cells." Suppression of aspirin appears to interfere with this process.

This is the first study showing the ability of platelets to modulate the expression of c-MYC in cancer cells. The researchers noted that nearly one third of colon cancer patients and 42% of pancreatic cancer patients show c-MYC oncoprotein overexpression. They also pointed out that aspirin has the same effect on platelets at both high and low doses. As a result, clinicians can weigh the risks and benefits of aspirin intake and reduce the risk of bleeding, which is a common side effect of taking too much aspirin. The authors underscored the key role of physicians and health care professionals in considering low-dose aspirin intake.

"Because the interaction between platelets and cancer cells occurs at an early stage, the use of antiplatelet doses of aspirin may be a safe and effective prophylaxis," the authors conclude. Flarebio provides superior recombinant proteins such as recombinant TLR2 for your research.

Scientists are trying to prevent transfer of cancer by blocking their energy source

According to research using recombinant rat proteins, scientists have found that cancer cells in cancer-bearing mice have a weakness - they need fat to make fuel. A team has found that blocking these cells to absorb fat can prevent the transfer of cancer in mice. They hope the same thing can happen on humans.

Now a new study adds strong evidence to this hypothesis. The researchers found that the energy sources of cells which are responsible for the spread of oral cancer in mice are fatty acids, including palmitic acid - a common food additive which is the main component of palm oil. They found that in many metastatic cells, a receptor protein called CD36 was expressed at a higher level, which helps the cells absorb fat. The high expression of CD36 is also associated with poor treatment outcomes in cancer patients, so the team decided to look at what would happen when the receptor is blocked. Incredibly, when the expression of CD36 in cancer cells is blocked, it can completely prevent the spread of human cancer in mice, but it did not prevent the formation of tumors.

"We hypothesized that the cells responsible for proliferation depend on a particular fatty acid and that they don't work without these fatty acids," Salvador Aznar Benitah, research leader, said, "But we don't yet know why CD36 would have prevented this effect."

The research team has a lot of work to do, and the current results show that this method can play a role when the cancer spreads. Inhibition of CD36 expression in mice reduced tumor diffusion by 15% and reduced tumor size by 80%. The study also found that mice with a high-fat diet made their lymph nodes and lung tumors bigger than the normal diet, which is a signal of tumor spread. What should be clarified is that this study only works for human cancer cells in mice, and it doesn't mean that the same method is also effective for humans.

At this stage, no one would suggest reducing fat intake in food to avoid the spread of cancer, especially for cancer patients who need high-energy diet to maintain health. The team is currently working on the development of human antibodies against CD36, hoping to carry out clinical trials in next 5 years.

"This is an exciting and very important first step," said Benitah, "And we have identified the cells responsible for metastatic cancer, which will be studied in more detail later. It opens up a new anti-metastatic therapy. We look forward to the end result of this study, because we have had many revolutionary new therapies for cancer treatment, but preventing its spread is unprecedented for the first time." Cusabio provides you with recombinant proteins of good quality such as recombinant TLR2 at good prices.

Scientists have found that Piezo2 protein prevents lung hyperproliferation in mice

Scientists have found through recombinant human proteins that Piezo2 protein prevents lung hyperproliferation in mice, according to a paper published online recently in the journal Nature. The findings will provide new insights into a number of respiratory disorders, such as sleep apnea and chronic obstructive pulmonary disease.

Most mammals prevent hyperproliferation of the lungs by a reaction known as the "He-Baum II reflex", which causes the inspiration to stop immediately. However, its specific working mechanism is not clear. Previously, no Piezo2 proteins were found associated with the respiratory system.

At this time, scientist Adam Patapatinian and his colleagues at the United States Scripps Institute explore the Piezo2 protein in regulating the role of lung expansion in mice. They found that deletion of the Piezo2 protein in adult mouse-specific neurons compromised the "He-Baum II reflex", resulting in increased tidal volume (i.e., greater intubation than usual), whereas neonatal mice lacking Piezo2 protein will die at birth.

These results show that Piezo2 protein can sense airway dilation, establish respiration in neonatal mice and regulate normal breathing in adult mice. This is essential for the initial expansion of the lung at birth.

The authors suggest that if the body of this expansion of the receptors defects, it will cause some respiratory disorder-related diseases, such as chronic obstructive pulmonary disease and sudden infant death syndrome. However, more detailed role of Piezo2 protein and the mechanism still needs further study. Flarebio offers good-quality recombinant proteins like recombinant TLR2 at competitive prices.

Scientists have summarized the newly-discovered molecular mechanism after antibiotic therapy

Scientists around the world are struggling to find a solution to the problem of bacterial multidrug resistance. A new study conducted by the University of Copenhagen using recombinant human proteins shows that even sensitive bacteria produce so-called "drug-resistant strains cells". A comprehensive analysis of this phenomenon helps to better select drug treatments and even stimulate new antibiotic to treat resistant infections of refractory strains.

In a recent issue of the journal Science, Alexander Harms and colleagues from the University of Copenhagen summarized the newly-discovered molecular mechanisms of chronic and recurrent infections caused by surviving bacteria after antibiotic therapy.

"The surprising resilience of bacteria is usually due to dormancy-like physiological state called persistence," says Harms. "At this point, bacteria are resistant to a variety of antibiotics and exogenous drugs. Bacterial cells can convert to bacterial persistence by activating specialized procedures. Once converting to bacterial persistence, the bacteria may be resistant to antibiotic therapy and can even be revived, resulting in recurrence of infection after cessation of antibiotic therapy."

Bacterial persistence, to some extent, is triggered by bacterial toxins that shut down important cellular processes (such as protein synthesis or energy production), forcing bacterial cells into dormant conditions so that they are no longer readily killed by antibiotics. Bacterial persistence is like hibernating animals or spores produced by mushrooms and plants.

These procedures of bacteria are controlled by a regulatory compound known as the "magic spot" and play a central role in bacterial persistence. These important findings will provide a basis for the development of new diagnostic tools and a more effective treatment strategy for a range of bacterial infections. Flarebio provides you with high-quality recombinant proteins like recombinant Ptpra for your research.

To understand the development of Alzheimer's through molecular structure

Scientists at the University of Washington School of Medicine have detailedly analyzed the molecular structure of Alzheimer's disease through recombinant rat proteins. Understanding the molecular structure (and the effect of genetic mutations on the molecular structure) can help to understand the development of Alzheimer's and other neurodegenerative diseases and how to prevent and treat them.

It has been recognized and supported that molecular TREM2 is related to cognitive decline and is a sign of neurodegenerative diseases, including Alzheimer's disease. In previous studies, some mutations alter the structure of TERM2, thereby increasing the risk of disease or developing Alzheimer's disease, dementia, Parkinson's syndrome, amyotrophic lateral sclerosis (ALS), etc. Other TREM2 mutations with a rare genetic disease Nasu-Hakola will lead to dementia, and most patients would not outlive 50 years old.

"We do not have an accurate picture of the effects of abnormal TERM2 on neurodegeneration, but we know that inflammation is a big threat in any case. And if we can master its own protein structure and how it affects its function, we are looking for ways to set things right." said the team leader.

TREM2 is located on the surface of the immune system of small glial, and it is called the important "housekeeper" cells. By phagocytosis, it forms β amyloid protein of Alzheimer's disease and other substances. If the microglia lacks TREM2, or if TREM2 is dysfunctional, the cell steward can't perform a cleanup task.

"What TREM2 has done remains unresolved, but we know that TREM2 can't keep the brain healthy in mice," says the team leader. "Now that we have understood the molecular structure of TREM2, we can go one step further to study its role in neurodegenerative diseases."

In addition, she added that TREM2 is also associated with a number of other inflammatory diseases, including chronic obstructive pulmonary disease and stroke. Therefore, understanding the structure of TREM2 can be important for the understanding of systemic degenerative diseases. Flarebio offers recombinant proteins of good quality such as recombinant Itgb1.

New progress in the research of protein structure and function under confinement domains

Recently, Li Conggang study group from Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences have made new progress in the research of protein structure and function under confinement domains. The results of the study are published in the journal Angew. Chem. Int. Ed, which also has other studies on recombinant rat proteins.

The confinement environment exists commonly in cells, such as molecular chaperone protein GroEL, ribosome peptide chain channel molecular machinery and a variety of organelle membrane gaps. It has been shown that confinement environments have an effect on the folding and stability of protein, but the effect of confinement conditions on the structure and function of multi-domain proteins is poorly understood.

Nuclear magnetic resonance spectroscopy is the most powerful means to obtain high resolution structures and functions of protein in complex environments. Researchers have used NMR to study the structure and function of the important signal transduction protein, calmodulin in simulated confinement environments.

The results showed that: 1) The structure of calmodulin was significantly different from that in dilute solution, in which calmodulin mainly existed in stretched structure and compact spherical structure in confined environment; 2) Calmodulin can interact with MLCK peptide, AcN19 peptide and somatostatin peptide. While in calm environment, calmodulin can bind to MLCK and AcN19 peptide and hardly bind to somatostatin peptide. Further studies have shown that the reason for the difference in function between the two environments is the spatial volume effect, not the difference in affinity. This study analyzes the high-resolution structure of the double-domain proteins in the first confinement environment, providing a structural basis for understanding the environmental effects of protein functions. At the same time, the study suggests that cells may use the restricted environment to regulate the function of some biological macromolecules.

Assistant researcher Xu Guohua and Ph.D. candidate Cheng Kayi are the co-authors of this article, and researcher Li Conggang is the communication contact person. Cusabio provides you with high-quality recombinant proteins such as recombinant CDH11 at competitive prices.

The new inhibition function of NOX4 protein in liver cancer

Researchers at the Bellvitge Institute for Biomedical Research (IDIBELL) in collaboration with King's College London have revealed the role of NADPH oxidase NOX4 as an inhibitor of epithelial amebiasis. This process helps tumor cells migrate and invade. The study was recently published in the journal Oncogene, which also publishes other studies on recombinant human proteins.

In previous studies, the researchers suggested that NOX4 acts as a tumor suppressor in the liver by inhibiting cell proliferation. "In this work, we demonstrate that NOX4 is also an important inhibitor of the invasion and metastasis of liver tumor cells," explains Dr. Isabel Fabregat, leader of the IDIBELL study group.

In-vitro studies have shown that NOX4 silencing in liver tumor cells induces amoeba migration motility. Deformation motions associated with cell shrinkage are regulated by the Rho family of proteins, and the increased expression leads to this type of movement, which is associated with aggressive metastasis.

In patients with hepatocellular carcinoma, a large number of cases were observed in the absence of NOX4. In addition, those patients with lowly-expressed NOX4 and highly-expressed Rho protein had worse prognosis. "This translates our in-vitro studies into translational correlates because it brings new prognostic biomarkers for this type of cancer," said IDIBELL.

NOX4 is regulated at the transcriptional level of TGF-β cytokines, which has been studied by the group for 15 years. TGF-β is known to be a tumor suppressor at an early stage, but it becomes an inducer at an advanced stage. According to previous studies by this group, when the expression level of NOX4 was high, TGF-β showed as inhibitors, so the use of inhibition of TGF-β drugs would be counterproductive. This study suggests that this type of drug can be an ideal candidate for patients when NOX4 is expressed at low levels and the expression level of Rho protein is high. "Thus, lowly-expressed NOX4 can be used not only as a marker of poor prognosis, but also as a marker for the use of TGF-beta inhibitors," Dr. Fabregat concluded. Flarebio offers good-quality recombinant proteins like recombinant Nrg2 for your research.

Scientists reveal the relationship between intestinal microbes and β cells

Recently, researchers led by renowned biologist Professor Karen Guillemin at the University of Oregon have brought a great breakthrough in research. They found that growth division of β cells may be controlled by gut microbes. It is well known that β cells are the only cells capable of secreting insulin, and the importance of this finding is self-evident. It is reported that this is the first time that scientists revealed the relationship between intestinal microbes and β cells. The discovery may increase a weapon for the diagnosis and treatment of diabetes. This important study by Professor Guillemin's team has been published in the famous open-source journal eLife, which also publishes other studies on recombinant rat proteins.

Professor Guillemin's team has not yet carried out research in the human body, but they did a guided study. They found several intestinal micro-organisms in the human intestinal, and they can secrete protein like BefA protein with different similarity. Hill then treated the zebrafish with the highest and lowest similarities, and he was surprised to find that zebrafish β cells also returned to normal levels. This suggests that a similar phenomenon is most likely to occur in the human body. Professor Guillemin's team is currently conducting in-depth research.

"Our research suggests that the growth and development of animals may be dependent on the release of intestinal microbial signals," Hill said, "It is too excited to see that the intestinal microbial glucose stability in glucose plays such an important role."

"We have spent many years isolating and studying the intestinal flora of zebrafish, and our efforts have not been in vain," says Professor Guillemin. "We found BefA proteins that can regulate the growth of β cells."

For patients with type I diabetes, their onset time is very early. At that time, the β cells are very fragile and vulnerable to be attacked. If the corresponding micro-organisms are then missing, it will make the patient's condition worse. Incidence of type 1 diabetes includes genes and the environment, including environmental factors and intestinal micro-organisms. Studies have shown that human β-cells generally enter dormant period in the 5-year-old and stop the division of growth. Therefore, early use of antibiotics in newborns may increase the risk of newborns suffering from type I diabetes.

Professor Guillemin said that they currently need to work with researchers studying type 1 diabetes to study the development of BefA molecules as a potential therapeutic approach. There are already many companies in the development of microbial transplantation for the treatment of oral disease capsule, hoping that the treatment of diabetes can also use similar products. Flarebio provides you with high-quality recombinant proteins including recombinant CDH2 for your research.

To promote the timely regeneration of cells by designing stem cell strategies

A team led by the National Child Health System reports that the brain developed in newborns has certain types of immature progenitor cells that can be expanded and induced to replace brain-injured cells. In a clinical model of early brain injury through recombinant horse proteins, Sirt1 plays a key role in the regeneration of glial cells by endogenous progenitor cells after hypoxia-associated brain injury.

Dr. Vittorio Gallo, director of the National Center for Neuroscience Research in Children, said, "It's not healing. It's about regenerating the lost substance." The first step is to identify cells that can regenerate the loss and then expand its associated endogenous cell proliferation. The percentage of glial progenitor cells in total brain cells was 4 to 5. Considering that the brain consists of billions of cells, this is a considerable number. The advantage is that these progenitor cells already exist, and there is no requirement through the blood-brain barrier, and ultimately they will differentiate into oligodendrocyte white matter and mature glial. That's exactly what we want them to do.

The team found that Sirt1 is a novel modulator of basal oligodendrocyte progenitor cell (OPC) proliferation and an important regulator of neonatal white matter hypoxia. "We also clarified the mechanism by which Sirt1 targets other members of the Cdk2 signaling pathway by modulating their deacetylation, complex formation, and E2F1 release, driving the Cdk2-mediated signaling pathway," said Li-Jin Chew, Ph.D., associate professor of research at the Children's Neuroscience Research Center.

In neonates, hypoxia-induced brain damage initiates spontaneous amplification of progenitor cells but also leads to a lack of mature oligodendrocytes. Inhibition of Sirt1 expression in vitro and in vivo indicates that loss of its deacetylase activity prevents the proliferation of OPC in hypoxia while promoting maturation of oligodendrocytes, emphasizing the importance of delicate balance of Sirt1 activity between maintenance of both processes.

Time is of essence because Sirt1 plays a beneficial role in a certain place (white matter) and at a given time (immature brain continues to develop). "We saw the largest Sirt1 expression and activity in the first week of neonatal brain injury," Gallo said. "There is a very narrow window that uses the stimulus of the amplified progenitor population to target this particular molecule for repair."

The team reports that Sirt1 is a nicotinamide adenine dinucleotide-dependent class III histone deacetylase, known to be involved in normal cell development, aging, inflammatory response, energy metabolism and calorie restriction. Its activity can be regulated by inhibiting the sirtinol protein of the off-the-shelf drug sirtinol. This finding points to the potential of therapeutic interventions for diffuse white matter injury in neonates. "Ideally, we would like to be able to promote the timely regeneration of cells by designing stem cell strategies," Gallo said. By the way, Flarebio offers superior recombinant proteins such as recombinant CDH2.

To develop novel CRF1 receptor inhibitors is important to treat neuropsychiatric disorders

According to research using recombinant dog proteins, CRF mRNA and CRF are widely distributed in the central nervous system (CNS) and abundant in the hypothalamic paraventricular nucleus (PVN), brainstem, amygdala, hippocampus and neocortex. CRF is a neuropeptide containing 41 amino acids. It is a kind of hormone that regulates the hypothalamic-pituitary-adrenal (HPA) axis of the hypothalamus. It is also the key hormone of neuroendocrine regulation in stress response.

CRF receptors are mainly two seven transmembrane G protein receptors (CRF1, CRF2). CFR and CFR1 have high affinity, but the affinity for CFR2 is weak. In the human body, CFR1 includes five subtypes of α, b, c-h, i, mainly distributed in the anterior pituitary, hippocampus, cerebral cortex and amygdala. Distribution of CFR1 in the anterior pituitary promotes the release of adrenocorticotropic hormone (ACTH) in the hypothalamus, which in turn promotes the release of cortisol from the adrenal cortex; which in turn regulates glucocorticoid receptors (GRs) and mineralocorticoid receptor (MRs) and the signal cascade mediates intracellular responses to stress.

Compared to CRF1, CRF2 is confined to discrete brain regions, such as the dorsal raphe nucleus (DRN), lateral septa (LS), and periaqueductal gray (PAG). CRF2 only has three subtypes: a, b, c. Although the role of CRF2 is less than CRF1, it can antagonize the CRF1-induced stress response. The different roles of CRF1 and CRF2 are also reflected in the distribution of DRN nerve cells. CRF1 is mainly in the cell membrane, while CRF2 is mainly distributed in the cytoplasm. Tension stimulation reverses this distribution, causing CRF to stimulate DRN cells rather than inhibition.

CRF1 and CRF2 have a variety of signaling pathways, the main pathway is CRF1 and CRF2 triggering downstream cascade signals leading to G protein activation, Gαs trigger second messenger cAMP (cyclization of monophosphate), cAMP activation of cAMP protein kinase A (protein kinase A, PKA). They also activate Gαq, activating the cascade of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) - mitogen-activated protein kinase (MAPK). They can also activate the apoptotic pathway through Akt / protein kinase B, NOS-guanylate cyclase and caspase. Because of this complexity, CRF1 may exchange signals through different channels of the signal.

With the further development of psychopathology, the role of CRF gets more and more attention. Numerous studies have shown that CRF levels are high in patients with neuropsychiatric disorders (including depression, addiction disorder, post-traumatic stress disorder, irritable bowel syndrome, generalized anxiety disorder, etc.) and they also found CRF mRNA increase in the tissues in patients. Subsequent studies have shown that patients are over-expressed in CRF mRNA, resulting in excessive production of CRF. Other studies have demonstrated that increased activity of the CRF1 receptor leads to the development of certain neuropsychiatric disorders. At the same time, it was also demonstrated that specific SNPs are also associated with depression. Therefore, to develop novel CRF1 receptor inhibitors is important for the treatment of neuropsychiatric disorders. Flarebio provides you with good-quality recombinant proteins including recombinant ECE1.

Researchers are trying to control senile dementia

The Dementia Research Center in the United Kingdom is trying to make dementia as controllable as HIV, and if the results are significant, we can see results in the next few years. This research using recombinant mouse proteins can help a lot of people tide over, solving the problems that have plagued the medical profession for decades.

"Alzheimer's disease is expected to be under control in 2025," the team leader said, "And this study can also help the brain reconnect and reorganize the memory system eroded by the disease."

Famous Belgium psychiatric experts expressed the hope in an interview with the Associated Press that the treatment of this disease can be treated as the same as HIV treatment. He said, "The brain is the most flexible tissue of our body. If we can control the disease early in the disease, the brain can slowly restore the lost function." The team consists of multidisciplinary teams of doctors, biologists, engineers, and data specialists.

Scientists also said that in addition to "amyloid hypothesis", the scope of the study can be further expanded. Amyloid hypothesis is a long-standing focus of research in this field. According to the Post, the brain aggregate agglomerate abnormal protein called amyloid beta plaques, causing the disease.

These plaques are hallmarks of Alzheimer's disease, but the purpose of their existence is not known. In addition to the "amyloid hypothesis", there must be other signs. Alzheimer's disease is not just the case. It is certainly like cancer which is caused by the accumulation of complex factors.

"The team hopes to change the way people know about the disease through a multidisciplinary approach in the first year," the Financial Times reported. Flarebio offers high-quality recombinant proteins like recombinant CDH15 at competitive prices.

To treat breast cancer spread with nanoparticles

Recently, the researchers found through research using recombinant horse proteins that nanoparticles can slow tumor growth so that the treatment of breast cancer more effective, and thus treating breast cancer spread.

The journal ASC Nano published the article entitled "using pRNA nanoparticles to overcome the tamoxifen resistance of breast cancer". Scientists have developed a multi-functional RNA nanoparticle which can promote the treatment of breast cancer.

Researchers used nanosecond delivery systems to treat tumor-growing proteins called MED1 and to treat her-2-positive breast cancer. In addition, they used moxifen to make cancer cells more sensitive.

"Most breast cancers have been shown to be estrogen receptors, the anti-stimulant drug moxifen has been widely used in the treatment, but the treatment is not satisfactory. Estrogen receptor-positive tumors are unresponsive to them, or they produce drug resistance after the treatment. "In this study, we have developed an innovative design that utilizes HER2 and MED1 for these tumors," reports from the Science Daily.

The team developed the nanoparticles which can effectively link HER-2 with breast cancer cells, so MED1 will gradually reduce. Researchers use these biosafety nanoparticles for use in animals.

"These nanoparticles, combined with Moxifene, have a dramatic effect on the treatment of breast cancer, which is known to play a crucial role in the proliferation, relapse and resistance of cancer cells. Eliminating these cells represents progress, and it also provides a more ideal treatment for breast cancer patients."

Researchers also said that the new discovery will be more effective for the treatment of breast cancer. Of course, more clinical trials need to be conducted. Flarebio provides superior recombinant proteins like recombinant ECE1 for your research.

To improve the therapeutic effect of cancers and HIV in new way

For a long time, retinoblastoma protein (pRB) has been studied in cell growth and cancer prevention. Now, in a new study, the scientists discovered a new role for pRB through research using recombinant human proteins, which not only enhances cancer efficacy, but also works to treat other diseases, such as HIV.

Most of the DNA that is recombined in the human genome is called "junk DNA", and these are relics of the past that usually do not play any role and are quietly present. If they start to copy, they will re-enter the human gene, bringing diseases such as cancer.

The team found that binding of pRB to another protein called EZH2 keeps these "junk DNA" in silence, whereas pRB acts as a vector. EZH2 is transported to a repeating sequence.

This new discovery breaks the cancer genetic experts' understanding of pRB and EZH2, and most researchers have never thought that these two widely-existing proteins in the DNA have such an effect. "This opens up a myriad of gates for the treatment of multiple diseases, including antitoxic drugs, which allow patients to have multiple choices during treatment," the researchers said.

The new study also shows that EZH2 inhibitors help the immune system find cancer cells. They can block EZH2 and wake up the "junk DNA", so the cancer cells will appear in the immune system, as if infected by the same virus. The immune system will target cancer cells and kill them.

The findings also help other diseases, such as HIV, are also "junk DNA" hidden in the immune cells. Because the immune system can't detect these "junk DNA", so the patients are always HIV positive. EZH2 inhibitors can make these "junk DNA" become lively and show themselves so that we can use the existing drugs on the market for treatment.

"Over the years, we have been working on pRB, but we have never thought about it, and it is now clear that the combination of pRB-EZH2 is effective in treating a variety of diseases," the researchers said. By the way, Flarebio provides you with good-quality recombinant proteins including recombinant CDH15 at great prices.

Scientists have discovered the key factor NLRC3 which inhibits colon cancer

Immunologists at the St. Jude Children's Research Institute in the United States recently discovered a key class of NLRC3 that inhibits colon cancer through recombinant human proteins. The research led by Thirumala-Devi Kanneganti, Ph.D., of the Department of Immunology was published in the recently published Nature journal.

In the initial experiments, the researchers found that the removal of protective NLRC3 protein increased the development of colon cancer and also confirmed the NLRC3 tumor suppressor pathway key molecules so as to protect the treatment of colon cancer mechanism and provides a new drug target. NLRC3 belongs to a class of NLR "receptor" molecules with the regulation of the immune system and other cytological functions. However, up to now, the development of NLRC3 inhibiting tumor is still unclear.

The researchers found that NLRC3 mainly play a role in colonic epithelial cells and can be directly against infection or tumor cell development caused by intestinal inflammatory response. "All of these experimental designs are complementary and can further help us to confirm the function of NLRC3, which is essential for protecting the body from the proliferation of abnormal cells." When the NLRC3 gene is missing, the tumor will develop "Suggests Kanneganti". This suggests that if we can find a way to clinically induce high expression of NLRC3, we can block the signaling pathways leading to tumorigenesis," Kanneganti said.

"The most important thing to improve the activity of the NLRC3 molecule is to precisely determine the signaling pathways and mechanisms involved in the regulation of this molecule in the cell," says Kanneganti. The researchers revealed that NLRC3 plays a "brake" role in the PI3K-mTOR pathway, which usually starts early in the development of the tumor. "The development of direct drug therapy for the PI3K-mTOR pathway is very difficult because the pathway is central to cell signaling," says Kanneganti. "Therefore, we can target the NLRC3 molecule itself to block early development of tumor cells."

Despite the preliminary clarity of the mechanism of action, the team believes that the role of NLRC3 not only to prevent the occurrence and development of tumors in some infectious and inflammatory diseases, there should still be a lot we don't know about the role. From a broader perspective, further in-depth study could elucidate the function of other NLR family members. "NLR family functions are diverse. They not only can regulate the immune system and inflammatory response, but also can block the tumor production process," Professor Kanneganti said, "No one would link NLR family protein and PI3K-mTOR pathway together previously, so this study makes people particularly excited, because it is likely to open a new door to studying the functions of NLR." Flarebio provides superior recombinant proteins including recombinant ECE1 at great prices.

Researchers discover new method of hijacking cells for viruses

DNA contains instructions on how cells make the desired substance. According to research using recombinant dog proteins, when cells need proteins, the relevant parts of the DNA will be transcribed, and transcripts called messenger RNA will leave the nucleus and enter the manufacturing machinery as templates to produce new proteins.

In this process, RNA can be edited in a variety of ways. It may be added to the additional instructions and may also be enemy control. Viruses can edit RNA information to create the version of the protein it needs to produce thousands of copies of the virus. Over the past few decades, biologists have a clearer understanding of how viruses hijack host cells.

Many viruses control the day-to-day running of cells by sending out messages that interfere with the ability to turn off unwanted cellular functions and enhance the functionality they require. But biologists at the University of California, San Diego, have recently discovered that there are some more hijacking mechanisms for viruses that are more subtle and more complex. They don't block cell information but change the content of the information.

The study is published in Nature Structural and Molecular Biology. By the way, Flarebio is a National High-Tech Enterprise with research, production and sales as one. Flarebio provides you with good-quality recombinant proteins like recombinant CDH15 for your research.

Scientists reveal the role of ARID1A in the regulation of active agent enhancers

Scientists have developed a set of model systems in mice through a lot of recombinant rat proteins, and it allows them to carefully observe how mutant proteins in human cancers play a role in tumor silencing. Not all cancers are caused by direct changes in the genetic code. Epigenetic events can also lead to abnormal gene expression induced by cancer. The study published in the Natural Genetics explains how the epigenetic process carries out gene regulation and induce colon cancer.

"The ARID1A mutation is widespread in human cancers and the development of experimental model systems is important to help us understand how gene mutations induce disease," said Dr. Charles W. M. Roberts, director of the St. Jude Children's Research Comprehensive Cancer Center.

ARID1A is an integral part of the SWI / SNF chromatin remodeling complex. Chromatin remodeling has a profound effect on gene expression. Chromatin remodeling of protein-coding genes in human cancers is the most common variant of the gene.

The researchers said, ARID1A can inhibit the tumor in the mouse colon, but it can't play a inhibition role in the small intestin. They found that penetration enhancers and shorter DNA regions are important components of the interaction of ARID1A with the SWI / SNF chromatin remodeling complex.

Scientists have revealed the role of ARID1A in the regulation of active agent enhancers, resulting in loss of control of the cellular identity ARID1A in the colon and inducing the formation of cancer.

The new model system will play a role in future work. "The systems we develop are important for understanding why dye modification mutations are so frequent in cancer, revealing the mechanisms that lead to colon tumor growth and studying potential therapeutic interventions." By the way, Flarebio offers good-quality recombinant proteins like recombinant CDH15 at good prices.

Experimental drugs can effectively prevent rejection of mice heart transplants

According to a new study by scientists at Weill Cornell Medicine and Brigham and Women's Hospital through recombinant human proteins, experimental drugs that block the activation of immune cell components effectively prevent rejection of mice heart transplants.

The findings published in the Proceedings of the National Academy of Sciences on December 12 describe a compound developed by medical researchers at Weill Cornell. The inhibits the cellular structure known as the immune proteasome while avoiding constitutive proteasomes. Proteasomes help cells to break down regulatory proteins to regulate their behavior. The constitutive proteasome is present in all cells, while the immunoproteasome is expressed predominantly in the cells of the immune system.

The currently-approved proteasome inhibitors also target two types of proteasomes. They are used in transplantation medicine to block immune cell function and reduce graft rejection. However, proteasome inhibitors in all cells of the body can cause toxicity in transplanted organs and hosts. The researchers demonstrated that their compound DPLG3, a highly selective and reversible inhibitor of the immune proteasome, only shuts down the immune proteasome, leaving the constitutive proteasome. DPLG3 reduces the number of immune cells in the graft. Inhibitors also increase the expression of "exhaustive markers" on the remaining immune cells. Exhaustive markers are typical of immune cells, reducing the ability to attack foreign cells. These changes protect the organ from rejection, while protecting the body from toxic side effects of non-selective proteasome inhibitors, such as bone marrow and nervous system damage.

"Transplant patients often have to take long-term toxic, broad-spectrum immunosuppressive agents, which increases the risk of infection, cancer and toxicity of the graft itself," said Dr. Carl Nathan, director of Department of Microbiology and Immunology and RA Rees Pritchet, professor of microbiology, and Cornell's professor of medical microbiology and immunology and medicine, "Selective blocking of the immune proteasome without affecting the constitutive proteasomes in other host cells and transplant organ cells can help patients to receive grafts on a long-term basis and improve organ transplants."

Medical researchers of Weill Cornell led by Dr. Gang Lin, associate professor of microbiology and immunology, co-author of the study, designed DPLG3, which is highly selective for the immune proteasome and is highly selective for long-term exposure. Dr. Nathan and Dr. Lin are co-inventors of the DPLG3 and have submitted patents. Flarebio offers good quality recombinant proteins such as recombinant PIGR at competitive prices.

New drug has been developed to treat lung cancer

According to a new study presented at the European Society for Clinical Oncology in Copenhagen, through research using recombinant horse proteins, researchers have developed a novel antibody that boosts the immune system against tumor cells. In patients with non-small cell lung cancer (NSCLC), it is more effective than conventional chemotherapy.

In Phase III clinical trials, patients who were not previously treated took the drug called pemumab and showed more frequent efficacy and longer lifespan. After 10 months, they developed a disease progression compared to receiving chemotherapy of the patients less. More specifically, compared with chemotherapy alone, the drug reduced the likelihood of cancer progression by half and reduced overall mortality by 40%.

The effect of this new drug is so good that scientists can't believe that they simply suspend the clinical trials so that all patients are replaced by this drug. Their clinical findings have been published in the New England Journal of Medicine. "Be mindful of this day. This is a new era of lung cancer treatment," researcher Stefan Zimmermann said in an interview in Lausanne, Switzerland.

Pemumab, developed by Merck, has been approved by the FDA as a second-line treatment for patients with advanced head and neck cancer, but its first-line treatment has not been confirmed. In an early clinical trial, a similar drug called naduzumab did not achieve the desired results, and the results showed that it was not more effective in the treatment of lung cancer than chemotherapy.

But the new clinical trial is specifically for NSCLC patients. Most cancer cells in these patients contain a protein called PD-L1 that prevents white blood cells from unnecessarily killing healthy cells, but also helps the cancer cells to be destroyed. According to the research team, about a quarter of NSCLC patients with advanced disease are consistent with this description.

Compared to traditional methods of care, pumu monoclonal antibody reduced the mortality of these patients by 40% in the experiment. In another small clinical trial, the researchers found that if combined paimuomab with chemotherapy, the effect is even more significant. Flarebio offers high-quality recombinant proteins like recombinant TLR2 at good prices.

Newly-developed drug for Alzheimer's disease is expected to come out

US researchers conducted a series research using recombinant mouse proteins and published a paper in the November 2, 2016, saying that they confirmed that the new drug Verubecestat in the clinical trial phase of Alzheimer's disease (AD) does not bring harmful side effects, and the effect of the drug as agentia is worthy waiting.

The study published in the US medical journal Science Translational Medicine refers, "From the beginning of the experiment that they began investigating 32 patients with varying degrees of Alzheimer's disease, now there are more than 3,000 patients participate in the experiment. The team also launched two comprehensive large-scale clinical trials."

In the treatment, the experts selected the compound Verubecestat developed by the US pharmaceutical company. Verubecestat is able to inhibit the BACEI enzyme and reduce the amount of β-amyloid.

One of the pathological features of Alzheimer's disease (AD) is the presence of amyloid plaques (β-amyloid deposits) in the brain. Such plaques not only severely affect memory, but also have significant influence on protein generation. Although BACEI enzyme inhibitors in the past have a certain effect, it often brings liver dysfunction, neuropathy and other serious side effects.

In this clinical trial, the specialists plan to verify the effectiveness of Verubecestat through three treatment stages. Now they have entered the third test phase and plan to draw the final test conclusions in July, 2017. If the results are good, then Verubecestat will enter market in 2-3 years as new treatment drug. By the way, Flarebio provides you with superior recombinant proteins like recombinant TLR2 at competitive prices.

Researchers are developing new drugs for the treatment of leukemia

The University of Southampton's cancer immunology study results in a drug that has been shown to reduce the risk of follicular lymphoma spread. According to the results of the Phase III GALLIUM study at the American Society of Hematology (ASH) Congress and research using recombinant horse proteins, a combination of Gazyva and chemotherapy in first-line therapy reduced the risk of worsening or death of blood cancer disease by 34%, while Rituxan plus chemotherapy can treat patients with follicular lymphoma. Gazyva was developed by Roche based on more than 10 years of immunological exploration and development of scientists at the University of Southampton.

Southampton researchers have found that therapeutic antibodies against this cancer target (CD20 on lymphoma) can be divided into two types: drugs that have already been approved, rituximab and Form II for Type I patients. Southampton studies have shown that if a Type II agent is prepared, it may be a better reagent because it can be retained on cancer cells for longer periods of time. Roche has developed the first therapeutic type II antibody, obinutuzumab, which has now been proven to be the best treatment regimen for Bilituximab, which is currently the best.

"Obinutuzumab can be found on the surface of malignant B cells," says Professor Martin Glennie, a professor of cancer immunology at the University of Southampton. "The CD20 protein can be used to label cells whose body is destroyed by destruction. It is a Type II agent, and the antibody has an advantage because it remains longer on the cell surface than previously-used antibody drugs."

The Phase III GALLIUM study led by the National University Hospital included 1,401 patients initially treated for asymptomatic non-Hodgkin's lymphoma, of whom 1,202 were follicular lymphoma. These patients were randomized to receive either ibuprofen or chemotherapy alone or with rituximab alone and with rituximab alone. The results also showed a 32% increase in relapse time compared with rituximab plus chemotherapy in patients treated with ibuprofen plus chemotherapy.

"This new approach to lymphoma antibody therapy begins with an immunological study in Southampton," said Peter Johnson, professor of medical oncology at the University of Southampton. "Starting with the discovery of how these antibodies work, this research lasted more than 10 years. We have more work to continue to explore in many different types of cancer, but this is a good example of how scienc providing better treatment for our patients." Flarebio provides you with good quality recombinant proteins including recombinant ITGB5 at reasonable prices.

To treat and prevent Alzheimer's disease by use of flash light?

Flash light can achieve removal of amyloid protein and reduce protein plaque generation and prevent and treat senile dementia, according research using recombinant human proteins. β-amyloid accumulation in the brain to form plaques is one of the hallmark of characteristics of the formation of Alzheimer's disease, and many currently-developed drugs take reducing brain β-amyloid levels as the goal. The field of drug development has been repeatedly hit, but the scientists did not give up β-amyloid plaques on the contribution of Alzheimer's disease. There are also scientists trying to take a more peculiar way to reduce brain β-amyloid accumulation. This week, the journal Nature published a study titled "Gamma frequencyentrainment attenuates amyloid load and modifies microglia". The researchers believed that brain electrical signal transients may lead to β-amyloid accumulation. Restoration of neural circuits to produce specific electrical shocks can reduce β-amyloid formation and activate immune cells to clear β-amyloid in the brain.

When the brain neuron network is activated synchronously, the oscillatory discharge is generated. This EEG frequency is 30-90 Hz, also known as γ-oscillation, which is thought to contribute significantly to high-level cognitive and perceptual responses. Authors such as Massachusetts Institute of Technology, Cai Lihui et al used the Alzheimer's mouse model to record neuronal activity. The results showed that after the decline in γ-amyloid protein accumulation of plaque formation, animal cognitive declined. They used optical genetics directly to stimulate neurons in the hippocampus of Alzheimer's model mice to produce γ-oscillations that significantly reduced β-amyloid formation in the brain region and activated microglia. Microglia is the brain immune cells, and it can remove β-amyloid protein after being activated.

The authors designed a noninvasive method of stimulating neurons in the brain. The mice were placed in a box filled with LED lamps and irradiated at a frequency of 40 Hz to visualize the primary visual cortex of the mice. The study found that this stimulus can reduce amyloid protein levels in the visual cortex of early Alzheimer's mice by 50% and reduce the number of amyloid plaques in the visual cortex of later-stage Alzheimer's mice.

The results showed that the frequency of 40 Hz can activate the microglia in the brain and improve the ability of amyloid removal, which can reduce the amyloid plaque formation, preventing and treating senile dementia. Treatment of Alzheimer's disease with γ-oscillations is a new therapeutic strategy, but whether it plays a role on humans needs to be further studied. By the way, Flarebio offers good-quality recombinant proteins like recombinant Ptpra at good prices.

Scientists find a protein that summons cell's gene-silencing machinery

It is known that organisms must defend themselves against parasitic genetic elements called transposons, from bacteria to humans, and the stake they undertake are high. These pieces of DNA jump around in the genome thus descripting genes. It can cause so much destruction that cells have dedicated surveillance mechanisms to keep them in check. Defects in these innate defense systems usually result in sterility. In animals, studies using recombinant horse proteins show that the main defense against troublemaking transposons is the Piwi-interacting RNA pathway.

In new research, scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Gregory Hannon, who is also a Professor and Senior Group Leader at the CRUK Cambridge Institute at the University of Cambridge, have identified a protein the Piwi system uses to guide a cell's gene-silencing machinery to the right spots in the genome, allowing it to keep transposons inactive without interfering with the organism's own genes.

Scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Gregory Hannon, who is also a Professor and Senior Group Leader at the CRUK Cambridge Institute at the University of Cambridge just conducted a new research, identifying a protein the Piwi system uses to guide a cell's gene-silencing machinery to the right spots in the genome, which allows it to keep transposons inactive and not interfere with the organism's own genes. They playfully named the protein Panoramix, after a comic book character who endows others with great power.

The Piwi-interacting RNA pathway, which is active in germline cells - those that give rise to sperm and eggs—is a double-tiered defense system. The most direct line of defense finds and chews up RNA copies of transposons, while a second mechanism finds transposons within the genome and tags them with chemical signals that instruct the cell to keep them safely off. The two modes of control provide the tightest possible clamp on the system.

The study of Hannon and his colleagues are currently focusing on the system that chemically tags transposon DNA. It happens as the elements are preparing to move, when transposon DNA is copied from its place in the genome into RNA, a process known as transcription.

According to Hannon, the Piwi system's challenge is to locate these sequences which look a lot like an organism's own genes, and tag them to make them be recognized by the same machinery a cell uses to switch its own genes off as needed. They think Piwi-interacting RNAs are responsible for finding transposons as RNA copies emerge, but the next was unknown. They hope to figure out the link between this very transposon-specific pathway to the more general repressive machinery of the cell.

They listed a lot of molecules which are possible to play this role and tested them. The Piwi system is so fast that they have found it nearly impossible to follow its components as they silence their natural targets. Later they constructed an artificial Piwi target, then stuck different components of the Piwi system to it and saw what was going on next.

For the most part, cells treated the piece of DNA that encoded the target as one of their own genes. However, when Panoramix was tethered to the artificial RNA target, it was able to halt transcription of the foreign piece of DNA. It means that once transcription began, Panoramix recruited the cell's gene silencing machinery to shut off local transcription and mark the intrusive DNA so that it would remain off, even in future generations.

It's a quite specific phenomenon. Panoramix summons the cell's gene-silencing machinery without affecting the activity of any of the fruit fly's own genes. The scientists believe that there may be a similar protein that plays the same role in humans and other animals. Flarebio provides good-quality recombinant proteins including recombinant Nrg2 for you.

Scientists are developing new drugs to remove deadly bacteria

The Group A Streptococcus (strep) infections are usually caused by a particularly nefarious strain - M1T1. One of the reasons for this name is the type of tentacle-like M protein projecting from the bacterium's surface. Despite that a lot of studies before proposed ways M1 might contribute to strep virulence and through researching using recombinant mouse proteins, researchers at University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences have given another explanation that is more persuasive than those ones: M1's ability to hold off antimicrobial peptides—natural antibiotics that comprise one of the immune system's front lines of defense.

The new study was published October 14 by Cell Host & Microbe. It emphasizes the importance of antimicrobial peptides, thus suggesting a new therapeutic approach to helping the immune system get rid of this crafty pathogen.

"The famous strep M1 protein has been shown to have numerous virulence properties that aid in bacterial colonization, fool the immune system or provoke inflammation," said senior author Victor Nizet, MD, professor of pediatrics and pharmacy. "We found that a major contribution of M1 protein to severe invasive infections can be explained by its ability to inactivate antimicrobial peptides."

More than 700 million infections all over the world each year, most notably strep throat and "flesh-eating" skin infections are caused by Group A strep. The body unleashes small antimicrobial peptides reacting to strep and other bacterial infections. These short chains of amino acids are deadly to bacteria in many ways such as summoning reinforcements in the form of infection-fighting cells or poking holes in bacterial membranes.

After research, the team found that Group A strep lacking M1 protein were easily killed by cathelicidin, a critical antimicrobial peptide. But they were rescued when armed with added M1 protein.

Besides, a research conducted on a mouse model showed that M49, a less virulent strain of strep, caused larger skin lesions in mice lacking cathelicidin than in normal, cathelicidin-producing mice. It means that M49 is unable to stiff-arm antimicrobial peptides the way M1 can, which makes the immune response more effective and the M49 bacteria less virulent.

The study stresses out the need to fortify or optimize antimicrobial peptides to improve the odds of defending infection of immune system. To know more about the interaction between M1 and antimicrobial peptides may develop new potential way of treating Group A infections. It's considerable to find an effective drug to help immune system fight against the infections by itself. Flarebio provides you with superior recombinant proteins like recombinant COLEC12 at good prices.

New potential treatment of tumor cachexia is coming

Recently, the international academic journal Molecular Therapy published the latest study results of Ding Qiurong Research Group from Chinese Academy of Sciences, Shanghai Institute of Life Sciences Institute of Nutrition Science, and the paper is titled "Prevention of Muscle Wasting by CRISPR / Cas9- mediated Disruption of Myostatin In Vivo". The aim of this study through recombinant dog proteins is to treat myosinophilia by CRISPR in muscle-specific target-knockout myostatin in response to severe muscular dystrophy in cancer patients.

Cachexia can be found in a variety of diseases, of which the cachexia associated with the tumor is most common. Tumor cachexia is a consumptive syndrome shown in many cancer patients, especially in late stages of disease. Although there are sufficient nutrient intake, the substantial loss of skeletal muscle also exist (with or without adiposity), leading to a serious decline in quality of life and survival.

In this study, under the guidance of researcher Ding Qiurong, Wei Yuda, a graduate student achieved used SaCRISPR / Cas9 to target the myostatin signaling pathways that are activated the effect of partly alleviating the cachexia in cachexia through the myostatin in body-targeted knockout muscles aiming at inducing myostatin signaling pathway. The main reasons for choosing myostatin as the target are: 1) myostatin signal pathway is the negative regulator of muscle growth and development. In addition to the muscular system, no serious adverse effects have been found in the natural individuals with myostatin function deletion mutations, and the safety of targeting has been guaranteed. 2) Early serial mice and clinical trials have demonstrated that the myostatin signaling pathway in cachexia (3) myostatin is mainly secreted by the muscle cells. The main mode of action is autocrine / paracrine mode, so the reduction in myostatin concentration in the muscle microenvironment can preserve some of the muscle function in the presence of cachexia.

Based on this, Wei et al. made use of muscle-specific promoter to start the expression of SaCas9 (staphylococcus aureus cas9) and then injected into the glandular-associated virus vector (AAV). After packed in mouse myostatin protein, significant recovery of skeletal muscle function was observed in the tumor-induced cachexia mice model (9% increase in mean skeletal muscle weight, 25% increase in average grip strength, and a slice at the injection site, compared to non-targeted mice staining found muscle fiber atrophy was significantly alleviated). This study as a confirmatory experiment suggests that the use of gene editing specific target knockout myostatin in muscle tissue can be used as a potential gene therapy for cachexia control and can further improve the in-vivo targeting efficiency, and a comprehensive assessment of targeted safety will contribute to its true clinical transformation. Flarebio offers recombinant proteins of great quality including recombinant CDH2 at good prices.

The impact of 128 AD-derived presenilin-1 mutations on β-amyloid production

Alzheimer's disease (AD) is the most common form of dementia, but the cause of AD is still poorly understood. Recently, Shi Yigong from Tsinghua University made use of a highly-purified recombinant γ-secretase to detect the impact of 128 AD-derived presenilin-1 (PS1) mutations on β-amyloid (Aβ42 and Aβ40) production. The results of the study were published in the Proceedings of the National Academy of Sciences (PNAS) in December. There are also other studies on recombinant human proteins published in the journal.

A hallmark of Alzheimer's disease (AD) is the accumulation of β-amyloid (Aβ) in the brain of the patient into amyloid plaques. Amyloid precursor protein (APP) is cleaved by an intramembrane protease gamma secretase, producing a different length of Aβ, where longer peptides are considered to be detrimental. Increasing the ratio of longer Aβs over short Aβs may lead to the formation of amyloid plaques and the consequent development of AD.

Another important indicator of AD development is the average age at onset (AAO) of patients with PS1, PS2 or APP co-mutation. A more deleterious mutation may be reflected in the lower AAO. Analysis of a small number of mutations in AD sources supports a strong correlation: the higher the Aβ42 / Aβ40 ratio, the lower the AAO. In contrast, a different set of PS1 mutations showed only a weak correlation. It is worth noting that these conclusions are derived from a limited number of mutations and lacks for statistical significance.

In this study, 138 human PS1 mutations were analyzed by reconstructing the mutant PS1 protein into γ-secretase containing APH-1aL and examining their ability to produce Aβ42 and Aβ40 in vitro. Approximately 90% of these mutations result in reduced production of Aβ42 and Aβ40. It is noteworthy that 10% of these mutations result in a decrease in the ratio of Aβ42 / Aβ40. There was no statistically significant association between the ratio of Aβ42 / Aβ40 produced by the γ-secretase variants containing the specific PS1 mutations and the average age at onset of the patient (the mutation was isolated from their body). By the way, Flarebio provides you with superior recombinant proteins such as recombinant CDH2 at great prices.

The attempt of developing new drugs for Alzheimer's disease has failed temporarily

A drug failed in a large trial of patients with mild dementia, while the drug was seen as an important test of the mainstream theory behind Alzheimer's disease. Critics of the amyloid hypothesis grapple with the results as evidence of their weaknesses. The hypothesis is that Alzheimer's disease is triggered by the gradual accumulation of amyloid in the brain. However, whether the theory can eventually produce a therapy is not yet conclusive. More research using recombinant rat proteins is needed.

Supporters of the theory say the latest trial involved a particular way in which the drug solanezumab works, rather than the defects inherent in the theory itself that could have led to this failure. At the same time, a number of trials are underway to test whether solanezumab or other drugs targeting amyloid proteins can be tested in people with Alzheimer's disease who are not yet symptomatic, or who already have the disease to play a role, although the latest results are negative.

As an antibody, Solanezumab can eliminate amyloid from the blood and cerebrospinal fluid. These proteins continue to form plaques in the brain. Eli Lilly, a developer of solanezumab, announced on Nov. 23 that it would abandon the drug as a treatment for patients with mild dementia. The result is a long list of promising treatments for Alzheimer's disease that have failed in the clinic, many of which target amyloid proteins, like solanezumab.

The Banner Alzheimer's Institute in Phoenix, Arizona, also tests three targeted amyloid-producing therapies in a population with a high genetic risk of Alzheimer's disease, one of which is also an antibody. "The results of Eli Lilly do not prove that amyloid hypothesis is false, and they add the importance of longer-term prevention trials," adds Eric Reiman, an experimental leader and lead author of the study. Flarebio provides you with high-quality recombinant proteins like recombinant CDH15 at competitive prices.

Hypertension is greatly related to Alzheimer's disease

Researchers at the Feil Family Brain and Mind Research Institute in New York recently published an article in the Journal of Clinical Investigation revealed that hypertension affects neurovascular regulation and recognition in the brain. Through research using recombinant human proteins, The mechanism of perivascular macrophage (PVM) has been found to play a key role in this process.

Studies have shown that long-term (14-day) infusion of ANGII in mice can cause a slow increase in blood pressure (to model hypertension) and cause brain neurovascular dysregulation, whereas the latter may affect brain recognition Knowledge function.

The researchers found that perivascular macrophages play an important role in the above-mentioned alterations in function, which is necessary for ANGII to cause neurovascular regulatory mechanisms. When mice were infused with ANGII for a long time, ANGII could cross the blood-brain barrier and enter the perivascular space. At this time, ANGII can bind to the ANGII-type receptor (AT1R) on the perivascular macrophage surface, enabling the latter to activate the NOX2-type NADPH oxidase, thereby catalyzing the production of reactive oxygen species (ROS) and causing damage to the brain Oxidative Stress in Regulatory Mechanism of Neurovascular. In contrast, short-term rapid infusion did not allow ANGII to cross the blood-brain barrier.

In order to better simulate human hypertensive conditions, the researchers used a chronic hypertensive mouse model strain BPH / 2J experiments. These mice have significant brain neurovascular regulatory mechanism abnormalities and cognitive dysfunction. The results showed that when the perivascular macrophages were clodronate clearance, the AT1R was blocked or ROS was cleared and the neurovascular regulatory mechanism abnormalities would be significantly reduced; perivascular macrophage clearance is more significantly to improve the cognitive function of mice.

This study shows that perivascular macrophages in the case of hypertension can occur under the oxidative stress caused by the inflammatory response, causing the brain neurovascular regulatory mechanisms and cognitive abnormalities of the brain, and it suggests that perivascular macrophages as the potential target of drugs are expected to reduce brain function due to high blood pressure and damage. Flarebio offers good-quality recombinant proteins such as recombinant PIGR for your research.

To treat rheumatic arthritis in a new way

A study led by researchers at the University of Birmingham reveals the key role of different types of fibroblasts in the development of rheumatoid arthritis (RA) using recombinant horse proteins, opening a new avenue for therapeutic research in this disease. Synovial fibroblasts (SFs) are cells that form part of the connective tissue or synovium, or artificial joint. In patients with rheumatoid arthritis, SF cells invade and attack cartilage and bone around the joint, causing injury.

A group of researchers at the Institute of Inflammation and Aging at the University of Birmingham identified two different types of SF cells within the synovial membrane. The team showed that these cell types (defined by the presence of specific cell surface markers PDPN and CD248) were aggregated in different layers of the synovium, and only one (PDPN typing) resulted in cartilage damage in RA patients.

During the course of the study, SF cells from RA patients were grown in an artificial synovium in vitro and then activated using stress-induced proteins called cytokines. An artificial synovial membrane containing SFs migrates into mice (whose own immune system has been "shut down"), while moving into human cartilage to mimic joints and see how SF cells develop in the body. After implantation, the test showed that the "lining" layer of the artificial synovium (i.e., closest to the cartilage portion) contained invasive PDPN-type SFs, while the distal part of the cartilage contained non-invasive CD248 typing.

The study also confirmed a recent finding that "activated" SF cells can migrate, that is, through the blood vessels to attack other in vivo cartilage. On the basis of these findings, the researchers showed that PDPN-typed SF cells migrated first and that CD248 cells only appeared in secondary tissues at later stages.

"This study not only shows the presence of different subtypes of synovial fibroblasts, but also suggests that these cells are able to self-infiltrate into the ‘lining’ and ‘sub-lining’ layers of the cartilage," said Dr. Adam Croft of the University of Birmingham who led the study. ”Combining the differences in cell mobility between the two cell types, these results have great potential in finding new therapeutic targets for rheumatoid arthritis."

The current treatment of RA is mainly to the patient immunosuppressive drug combination, may seriously affect the quality of life. The results of this study show that the SF cell process for the method not only make future treatment more effective but more easily accepted by patients. Flarebio offers superior recombinant proteins like recombinant Aoc3 at great prices.

The discovery and development of target probe of proteins

As one of the most abundant biological macromolecules, protein is the main performer of biological function and plays a key role in all kinds of life activities. Scientists have been exploring the application of protein manipulation tools in the living environment through recombinant human proteins in order to achieve the goal of protein structure and function of in-depth study, which has become one of the frontiers of the field of chemical biology. Many research groups in China have realized the specific activation of proteins through chemical decoupling technology, two-photon and near-infrared control technology and targeted small molecule probes and studied the molecular mechanism of cell signal transduction process.

In the field of chemical decoupling technology, Chen Peng's group put forward a new strategy of rational design of small molecule activator by combining non-natural amino acid fixed-point insertion technology and biological orthogonal "chemical decoupling" reaction. For example, protein kinase-mediated phosphorylation is a key process in cellular signal transduction and has a major influence on most physiological activities. However, the molecular mechanism of many kinases under normal physiological and pathological conditions is unclear. The use of small molecule activators can be used in kinase signaling studies to obtain new information. "We activate the 'effector protein OspF' in living cells and found that this protein causes 'phosphorylated Erk protein' in the nucleus to undergo a 'nuclear transport' mediated by irreversible dephosphorylation," said Chen.

In recent years, protein light-control technology has become another powerful tool to study cell signal transduction. Compared with the UV-excited probe, the two-photon-excited probe can greatly reduce the cytotoxicity and has broad application prospects. Liu Lei group from Tsinghua University took protein synthesis as the core technology to develop targeted immune protein light-control probe and made use of newly-developed protein probe of the immune cells in precise space-time stimulation of directional movement. This probe will provide an ideal molecular tool for understanding and controlling cell localization and localization-related cellular life activities in living tissue. Chen Xing group from Peking University has developed the use of near-infrared light activation and regulation of cell signal transduction pathway of the new method.

Yang Yi, a research group of East China University of Science and Technology used the natural photosensors to construct a light-controlled gene expression system for the targeted protein production and degradation. In the experiment, the researchers used the light to the live cells or the living animal protein production level carries precise control on time and space, successfully controlling the production of the insulin in diabetes mellitus body and the blood sugar concentration.

Li Yanmei research group from Tsinghua University used adjustable protein degradation strategy to achieve the target protein level within the cell decreased in order to achieve the purpose of reducing its activity. The researchers focused on the phenomenon of abnormal "non-enzymatic protein Tau" in the brain of Alzheimer's disease and used the "recognition-cutting" strategy to control the content of these proteins in cells. Flarebio provides you with good-quality recombinant proteins including recombinant TLR2 at good prices.