A new drug may be promising to treat breast cancer

A clinical trial of an antibody-drug conjugate that combines the active portion of a chemotherapeutic agent with an antibody that targets a molecule expressed on a tumor cell seems to be promising for the treatment of metastatic triple-negative breast cancer. The results of Phase 2 clinical trials of Sacituzumab govitecan (also known as IMMU-132) have been published online in the Journal of Clinical Oncology, which also publishes other studies on recombinant human proteins.

"This approach may represent a new treatment model for this refractory disease," said Aditya Bardia from the Massachusetts General Hospital (MGH) Cancer Center.

Tri-negative breast cancer - a tumor that does not have an estrogen or progesterone receptor and which expresses HER2, is an aggressive tumor that usually affects young patients and African Americans. Chemotherapy is a standard treatment regimen, but only 15% to 20% of patients with metastatic disease react. The average survival time is 10 to 13 months.

Sacituzumab govitecan combines antibodies targeting Trop-2 with SN-38 (chemotherapeutic agent irinotecan active metabolite). Animal studies of such antibody-drug conjugates have shown a high potency for implanted tumors that deliver a larger dose of SN-38 directly to tumor cells that have little effect on normal tissues.

The JCO paper reported 69 patients with metastatic triple-negative breast cancer. All patients in this study received at least one treatment, and most patients received several treatments, averaging 5 times. The protocol requires intravenous administration of the drug on days 1 and 8 of the 21-day cycle.

At the end of the study in August 2016, 21 subjects had achieved tumor size reduction of 30% or more (two cases achieved complete remission), of which 9 patients were treated for at least 12 months. Almost 70% of the participants had measurable tumor shrinkage. Less than two months after treatment began to respond, with an average of nine months, of which three lasted about 20 months. The overall survival was 16.6 months on average. Side effects such as nausea, alopecia and leukopenia are usually modest and are controlled by appropriate supportive care. Flarebio offers high-quality recombinant proteins such as recombinant CDH2 at competitive prices.

Scientists find same proteins in aging cells and cancer cells

According to a study involving recombinant rat proteins by Queen Mary University in London, proteins have played an unknown role in aging cells, and the researchers hope that this finding will play a role in the treatment of aging and early cancer.

The organs and tissues of our bodies are made up of a large number of cells that interact to regulate the body's function and to remain healthy. However, some of the same "abnormal" cells have been found in cells of aged cells and early cancer patients.

The study captures the increasing number of "aging" cells that affect the function of the tissue. And when the aging cells fail to proliferate, they try to communicate with neighboring cells, and the route of communication is primarily to release inflammatory proteins. The study published in the study Cell Report describes the method of aging cell exchange through integrin membrane proteins which includes a highly-expressed "integrin β3" protein in the aging cells.

"This is the first time that integrin β3 has proven its role in the aging process, and this research contributes to the future treatment of early cancer and aging," the researchers said. By the way, Flarebio provides you with superior recombinant proteins including recombinant CDH2 for your research.

The protein CD151 can improves the prognosis of ovarian cancer

Ovarian cancer researchers have identified protein biomarkers that are expressed on the surface of tumor cells in highly serous ovarian cancer (the most common and lethal subtype of the disease).

The main author Mauricio Medrano, molecular biologist and researcher at the Princess Margaret Cancer Center, has published his findings in a cellar journal which also has published other studies on recombinant human proteins. The study shows that patients with a high level of biomarker CD151 had a poor prognosis reaction.

"Ovarian cancer is caused by a variety of diseases," Dr. Medrano said. By identifying the potential role of CD151 and its survival in cancer cells, we hope to develop a treatment to target it as a marker of poor prognosis to further study to acquire the potential to develop a clinical screening tool, helping to individualize cancer treatment.

The study was led by lead researcher Robert Rottapel, and the study team also includes senior scientists and professors from the Department of Medical Biophysics and Immunology at the University of Toronto.

In a laboratory experiment, the team used cell lines from 40 patient tumor samples to determine whether CD151 could contribute to the survival of highly serous ovarian cancer cell sources. The team further analyzed the population of approximately 1,000 patients to establish a high level of link between CD151 and poor prognosis.

Dr. Medrano said, "For the scientific community, our research provides a lot of new information about other possible targets, not just CD151, which may be important and can provide new ideas on how to target ovarian cancer." By the way, Flarebio offers high-quality recombinant proteins like recombinant CDH2 at competitive prices.

Scientists have released pathogenic molecular mechanism of autism

Wu Bailin research group from Harvard University Boston Children's Hospital and Fudan University and Qiu Zilong research group from the Chinese Academy of Sciences Institute of Neuroscience completed a study to reveal the pathogenic molecular mechanism of autism. Related research results have been published online recently in the journal Molecular Psychiatry, which also has other studies on recombinant human proteins.

Autism is a complex hereditary syndrome and neuropsychiatric development of disease mostly in early childhood and there is no effective drug treatment. The study of basic and clinical research on autism and related animal models has become one of the hotspots in the field of medicine and neuroscience.

The researchers screened nine missense mutations of the DYRK1A gene in autistic patients and studied the function of Dyrk1a in the process of cell growth and cortical development by constructing mutant Dyrk1a. It was found that Dyrk1a plays an important role in the process of neurodevelopment, and the two nonsense mutations associated with autism have led to a functional loss of the DYRK1A protein.

The study suggests that the genetic mechanism associated with the disease is very complex, and the DYRK1A gene located on chromosome 21 is one of the autism candidate genes identified in recent years. The gene is well known for its role in Down's syndrome. Exon sequencing data show that autism patients also detected DYRK1A gene mutation, so the degree of correlation between this gene and autism has become an urgent scientific question which needs to be answered.

To this end, the researchers constructed the wild type, Dyrk1a_shRNA and nine mutant Dyrk1a plasmids of the gene. And the control group was expressed in mouse cortical neurons, rat hippocampal neurons and in vivo embryonic cortical cells, and they observed the growth and development of various types of cells.

The study firstly provides a functional study of neurodevelopmental-related mutations in DYRK1A, an important autistic candidate gene, which provides an important basis for further study of DYRK1A gene function and the pathogenesis of pathogenic molecules for autism. Flarebio offer high-quality recombinant proteins like recombinant CDH2 at competitive prices.

IRS-1 is essential for smooth muscle cells that make up veins and arteries

Diabetic patients have a high risk of heart disease. In spite of knowing this, scientists are still trying to use recombinant mouse proteins to track the specific biological causes behind this risk or to find ways to intervene. Researchers at the UNC School of Medicine are now searching for a possible culprit - a protein called IRS-1, which is essential for smooth muscle cells that make up veins and arteries.

According to a study published in the Journal of Biochemistry, too little IRS-1 causes cells to revert to "dedifferentiation" or stem cell-like states, and this may form plaques in the heart arteries, a disease known as atherosclerosis. The disease increases the risk of heart attack, stroke and other forms of heart disease. "When diabetes is under mismanagement, your blood sugar rises and the amount of this protein decreases, so the cells show abnormal proliferation."

The study focused on the formation of venous and arterial wall cells called vascular smooth muscle cells. The main function of these cells is to shrink each time the heart beats, helping to push oxygen-enriched blood to the body's tissues. When the plaques accumulate along the arterial wall, these cells gradually lose their ability to contract.

In the new study, the team found that IRS-1 was an inhibitor of abnormal signaling pathways, thereby maintaining vascular smooth muscle cell differentiation or localization. In the absence of IRS-1, the cells return to the stem cell-like state, which in turn activates abnormal signaling pathways and promotes cell proliferation.

In diabetic patients, the presence of IRS-1 is affected by the effectiveness of blood glucose levels or blood glucose levels. Previous studies have shown that IRS-1 is significantly reduced in patients with frequent or persistent hyperglycemia. The new study is the first to link this reduction with heart disease.

The next step, Clemmons Lab will look for substances that can stimulate this protein synthesis even in the presence of hyperglycemia. The results suggest that drugs that promote the promotion of IRS-1 can counteract the deleterious effects of hyperglycemia on atherosclerosis.

Clemmons said that the activity of IRS-1 may also play a role in other diabetic complications, such as eye and kidney diseases. Researchers plan to study these potential links. By the way, Flarebio provides you with recombinant proteins of good quality such as recombinant CDH2.

It is promising to find radical cure of inflammatory diseases

Scientists from institute have revealed that dead cells release effective inflammatory molecules that trigger inflammation in necrotic disease. The discovery can produce new and existing drugs that target molecules to be studied as a way of treating inflammatory diseases such as psoriasis and inflammatory bowel disease. The results are published in the Journal of the National Academy of Sciences, which also has other studies on recombinant human proteins.

The studies led by Dr. Lisa Lindqvist, Dr. Kate Lawlor, Dr. James Vince and Dr. Stephanie Conos have shown that interleukin-1β (IL-1) triggers inflammation during necrotic death. Death is important to protect us from infection by sacrificing infected or diseased cells for greater benefit. However, necrosis becomes inappropriate, triggering a damaging inflammation that causes an inflammatory disease.

Dr. Lindqvist said the discovery challenged a long dogmatic that inflammation caused by necrosis was a byproduct of dead cell debris. "Our study has determined that death cells release IL-1, a strong inflammatory signal in the autopsy process. Now we have found that IL-1 is the 'root cause' of necrosis-related inflammation," Dr. Lindqvist said. "We speculate that targeting this molecule may be an effective way to treat inflammatory diseases."

The results suggest that targeting IL-1 can inhibit inflammation associated with a variety of inflammatory diseases, including multiple sclerosis, ischemia-reperfusion injury, atherosclerosis, liver disease, pancreatitis, psoriasis, inflammatory bowel disease and infectious disease. "Our research suggests that the existing drugs that prevent IL-1 may help to treat these diseases," Dr. Lindqvist said. "We are also exploring how IL-1 is secreted by autopsy so that we can create new drugs to prevent its release and reduce inflammation to treat inflammatory diseases." Flarebio offers high-quality recombinant proteins like recombinant CDH2 at competitive prices.

The molecule which can inhibits activity of the protein related to pancreatic cancer

Early diagnosis of pancreatic cancer is difficult and lacks specific drugs. Recently, according to research through recombinant horse proteins, researchers from France and Spain have found a substance that has been used to treat anxiety can interfere with the development of pancreatic cancer.

Pancreatic cancer is one of the deadliest tumors. At present, it is generally treated through chemotherapy program. Nupr1 protein belongs to the "intrinsic disorder protein". As early as the 20th century, 90 scientists have pointed out that it is involved in the development of pancreatic cancer. Now, scientists have discovered molecules that can inhibit the activity of this protein.

Experts have shown that this study has been selected from among more than 1,000 drugs that have been approved for the treatment of various diseases to screen for the effective inhibition of Nupr1 activity. Through the combination of computer simulation and pharmacological test, it can be seen that this molecule can interact with Nupr1 protein. In-vitro experiments show that it can reduce the ability of tumor cells to activate and transfer and completely inhibit the possibility of colony formation. The active compound has been tested for efficacy in animals and has been shown to prevent the development of the disease. This compound is trifluoperazine.

Trifluoperazine was previously used only as an antipsychotic in clinical practice, demonstrating its excellent anti-tumor effect. The study has a new shift in the direction of treatment of pancreatic cancer. Inhibition of Nupr1 may become a new treatment device for the treatment of the pancreatic cancer. By the way, Flarebio provides you with recombinant proteins of good quality like recombinant CDH2.

Scientists have found new target of treating blood cancer

A proteoglycan molecule called CD99 is frequently found in stem cells from patients with blood cancer, including acute myeloid leukemia (AML) and associated myelodysplastic syndrome (MDS). The detailed report was published in the January 25 issue of the journal Science Translational Medicine. Based on this finding, the researchers designed an antibody that recognizes and disrupts CD99-coated leukemic cells, which have now been demonstrated in human and mouse cells. Antibodies are immune proteins that attach to specific targets, just like proteins that invade viral surfaces. In recent years, researchers have been able to control antibodies so they can target pathogenic molecules by conducting research involving recombinant horse proteins.

"Our findings not only confirm new stem cell molecules that drive human malignancies, but also show that these antibodies can kill human AML stem cells directly," the researchers said.

Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are caused by abnormal stem cells in the bone marrow, and patients show anemia, an increased risk of infection and bleeding. The findings are based on an understanding of cancer. Just as normal tissue, including stem cells causing other cells, this "cancer stem cell", is a major factor in many types of cancer. In AML, a small percentage of leukemic stem cells can't grow into mature red or white blood cells. Most of the initial treatment of leukemia is significant, but it often relapses.

The researchers were interested in CD99 in the observation of AML and MDS cells. Previously, CD99 was crucial for the rare bone tumor of Ewing's sarcoma, so the researchers wanted to find out the effect of CD99 on blood cancer. After comparing 79 AML patients and 24 MDS patients, the researchers found that about 85% of the patients showed high levels of CD99. High levels of CD99 were able to separate diseased stem cells from normal stem cells. The researchers then designed the antibody and bound it to CD99. It was found that when the antibody binds to CD99 on the surface of cancer cells, it sends a signal to the inside of the cell to increase the activity of SRC-family kinase.

"With the appropriate support, we believe we can quickly identify the best antibodies for patients and begin clinical trials," the researchers concluded. By the way, Flarebio provides you with superior recombinant proteins like recombinant CDH2 at good prices.

A new method to treat patients with hereditary immunodeficiency

Scientists have developed a new approach using recombinant mouse proteins to repair the defective gene in hematopoietic stem cells in patients with hereditary immunodeficiency - X-linked chronic granulomatous disease (X-CGD), according to foreign media reports. Scientists transplanted stem cells into mice that had been repaired and developed into white blood cells with normal function, demonstrating that they could be used to treat patients with X-CGD disease.

X-CGD is a hereditary disease with limited therapeutic options. It is caused by mutations in the CYBB gene, which can cause NOX2 protein deficiency and damage the ability of leukocytes to resist infection. X-CGD patients in vivo white blood cells can‘t kill bacteria, so they are susceptible to infection, threatening the safety of life. In the latest study, scientists from the National Institute of Allergy and Infectious Diseases (NIAID) under the National Institutes of Health focused on mutations in the CYBB gene in which a single change in the genetic code resulted in loss of activity of the NOX2 protein.

The researchers isolated hematopoietic stem cells from two patients and used a gene-editing technique, CRISPR-Cas9, to target and repair this mutant gene. This targeted gene repair method can be defective CYBB gene sequence back to normal human sequences. It is difficult to distinguish between correct genes and normal genes. In the process, the researchers didn't detect CRISPR-Cas9 gene editing technology to produce any unexpected effect. In contrast, other methods of restoring the function of mutated genes often lead to additional changes, including genetic material additions or losses.

The researchers also transplanted stem cells from X-CGD patients into immunodeficient mice and found that these stem cells did not produce adverse effects and that they could differentiate into leukocytes and produce functional NOX2 for up to five months. The study published in the journal Science Translational Medicine suggests that although they need further research, they are now able to provide a theoretical demonstration that this gene-editing method can repair hematopoietic stem cell gene mutations caused by some minor ailments.

Scientists are planning to carry out the next step. The ultimate goal is to use this method for X-CGD patients in clinical treatment. At the same time, they also said that this gene editing method is also applicable to other blood diseases caused by single gene mutation, such as sickle cell anemia. By the way, Flarebio provides you with good-quality recombinant proteins like recombinant CDH2 at good prices.

The dual life of cancer protein Dab2

According to research using recombinant mouse proteins, sometimes proteins play more roles than we expect. For example, Dab2 has been considered to be associated with cancer. This molecule is associated with a series of signaling proteins called the Ras-MAPK pathway. In many cancers, the components of Ras-MAPK mutate and begin to tell cells to grow out of control.

Dr. Xiang Xi Xu (Michael), a professor of cell biology at the University of Miami's Miller School of Medicine, discovered the Dab2 protein more than 20 years ago and has been studying its relationship with cancer since that time, according to researchers at the Sylvester Comprehensive Cancer Center in the United States. But now he has found that Dab2 has always been very low-key secret - it may have an important public health impact on the fight against obesity. In a study published in Scientific Reports, Xu's lab found that young mice without Dab2 did not experience weight gain when ingesting too much food. "These mice look normal and everything seems good unless we give them a high-fat diet," Xu said. "They just do not get fat."

The underlying mechanism may be around adipose-derived stem cells: immature cells, which can be split into more stem cells or differentiated into mature adipocytes. In normal mice, Dab2 inhibits Ras-MAPK, which in turn promotes a protein called PPA R. It helps in the differentiation of adipose-derived stem cells into mature adipocytes. Eliminating Dab2 can shorten this process.

Normal mice fed a high-calorie diet gained weight, knocking out Dab2 to keep mice slim - but only temporarily. As the mice mature, the metabolic effects dissipate. At six months, the Dab2 deletion had little effect. Xu believes that this is because mice (and humans) lose fat stem cells at maturity. This early impact may help to explain "why early weight problems may persist into adulthood and why many adults are so difficult to lose weight".

"Dab2 controls a group of adipose-derived stem cells that are slowly disappearing," says Xu. "It appears that children are particularly susceptible to eating, and they may increase the number of adipocytes and fat cells at a young age, and they can still make fat later in life. But the existing fat cells are growing, and childhood habits may affect adults, making them more prone to obesity.

From a public health perspective, these findings may reinforce the importance of "guiding children away from high-fat diets". This role of Dab2 has been identified and may lead to new drug strategies to combat childhood obesity as the protein may be an attractive target for drug development. By the way, Flarebio provides you with high-quality recombinant proteins including recombinant CDH2 for your research.

The key gene which promotes breast cancer development

Why does breast cancer develop? Why do some patients resist the established treatment? Researchers at the University of Basel have gained new insight into the molecular processes of breast tissue. Through recombinant human proteins, they identified the tumor suppressor gene LATS as a key participant in breast cancer development and resistance in therapy. The findings were published in the January 10 issue of Nature.

About one-third of patients do not respond to treatment or produce resistance. So far, it has not been possible to accurately predict which patients will respond to this treatment because scientists have not yet fully understood their underlying molecular mechanisms. In a comprehensive molecular study, a team of scientists led by Professor Mohamed Bentires-Alj from the Department of Biomedical Sciences at the University of Basel now has identified an important participant called LATS. They demonstrated how this enzyme works with other proteins and how it affects the development and treatment of breast cancer.

Researchers are working on genes that inhibit the normal growth of cancer cells. In particular, they studied the tumor suppressor genes LATS1 and LATS2. Once the LATS is removed, the process in the breast tissue changes. After removal of LATS, the number of luminal precursor cells in the mammary gland epithelium increased. Luminal progenitor cells are the origin of most types of human breast cancer cells. "LATS balances the fate of cells in mammary tissue. And when it does not, the balance is broken, causing tumors to develop," Bentires-Alj explains.

In healthy breast tissue, LATS brings together estrogen receptor α and protein degradation mechanisms. Without LATS, the receptor can no longer be properly degraded, which has an adverse effect on cancer therapy. "We demonstrated that LATS-free cancer cells no longer respond to Fluvestrant, an agent that promotes the degradation of these estrogen receptor antagonists," said Bentires-Alj.

The removal of LATS also stabilizes the proteins YAP and TAZ, both of which are upregulated and promote cell proliferation in many cancers. "As we gain new insight into the molecular processes of healthy breast tissue, we now have a better understanding of how cancer cells are expanded, and why certain tumors are resistant to treatment," Basel scientist Bentires-Alj concluded. Flarebio offers recombinant proteins of good quality like recombinant CDH2.

New cardiac stem cells which have great treatment potential

Researchers from North Carolina State University and the First Affiliated Hospital of Zhengzhou University in China have developed a new version of a new cardiac stem cell (CSC), according to a new study involving recombinant mouse proteins and it has been published in the International Journal of Nature Communications. These synthetic cells can provide therapeutic potential compared to natural stem cells, while reducing the risk of disease associated with stem cell therapy. In addition, the new stem cells developed by the researchers also have some stability, and this technology is expected to help to develop other types of stem cells.

Stem cell therapy can play a role in promoting endogenous repair of the body, that is, it can repair damaged tissues by secreting paracrine factors, including proteins and genetic material. When stem cells therapies can be effective in the treatment of disease, they often tend to induce tumor growth and immune rejection. What's worse, these stem cells themselves are very fragile. Before being used, they need to conduct a series of important processes.

"We developed a new version of heart stem cells, and these stem cells can be used in a variety of off-the-shelf applications," said Ke Cheng, co-author of the study. Researchers have developed a cell-derived microparticle (CMMP) that utilizes poly (lactic-co-glycolic acid) (PLGA). PLGA is a biodegradable and biocompatible polymer. Then researchers obtained growth factor protein from human heart stem cells and added this growth factor protein to PLGA, finally successfully covering these PLGA particles with the heart stem cell membrane. "We can package 'cargo' and stem cell shells into biodegradable particles," Cheng said.

In vitro, both CMMP and heart stem cells have been shown to promote cardiac muscle cell growth. CMMP has also been tested in a mouse model of myocardial infarction and found that CMMP binds to cardiac tissue and can promote growth after the onset of heart disease, and this effect is considerable with the repair role of heart stem cells. Due to a special structure, CMMP can't replicate, which reduces the risk of tumor formation.

The researchers pointed out that these new synthetic cells have the same principle with inactivated vaccines. While outer membrane structure can also help to bypass the body's immune response, which combine with the heart tissue, releasing special growth factors for repair. But these new stem cells can't self-replicate, so it will be able to repair the body tissue to produce a stable effect while at the same time with lower risk. These new stem cells are more durable than human stem cells and are well tolerated by repeated freezing and thawing. Scientists don't necessarily have to acquire these cells from human cells. The development of these cells is also applicable in other stem cells.

Finally, the authors hope that this study will provide a new basis for the development of more novel stem cell products in the future, and the development of new stem cell products will of course provide beneficial stem cell therapy for patients while reducing the risk of other complications. Flarebio provides you with recombinant proteins of good quality such as recombinant CDH2.

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.

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.

To make use of protein-protein interaction network

The largest database of protein-protein interaction network has been laughed today, according to EurekAlert!, a science and technology news sharing platform of the American Association for the Advancement of Science (AAAS). The database is a collection of more than 62.55 million protein-protein interactions. Wit this data resource and recombinant proteins such as recombinant horse proteins, researchers can elucidate the effects of multiple genes on disease progression.

The importance of mapping large-scale protein-protein interaction network is widely recognized, but the data are scattered across a variety of academic articles. Researchers from the United States, Denmark and the United Kingdom collaborated and integrated more than 43,000 published articles from the data and created the database named InWeb_InBioMap.

"Modern genetic technology makes it possible to sequen- tally the genome of patients with cancer or mental illness on a regular basis, but understanding the cellular systems affected by the genetic genetic variation remains a major challenge," said team leader Dr. Kasper Raj. A more complete map of the physical interactions of human proteins will enable us to explore more precisely the cellular processes affected by the disease than ever before."

Li Taibo, a co-editor of the team, explains, "It is just like human society, proteins like to work in small groups. The social networking platform Facebook can infer people who might know each other, based on interaction patterns and interest sharing between networks, as well as between protein-protein interactions." By exploring possible pathways of protein-protein interactions, the genome and molecular pathways can be deduced, thereby deepening the understanding of life processes occurring in human cells. Clinicians can use this to look at patterns of genetic data and provide new molecular perspectives for finding new disease-causing genes.

The team is also continuing to develop other uses of the resource database, such as integrating proteomics, transcriptome and genomic data to improve understanding of complex biological systems, and the use of this information will help to understand cardiovascular disease, birth defects, cancer, reproductive disorders, mental illness and other pathogenic mechanisms. Flarebio offers superior recombinant proteins like recombinant CDH2 at competitive prices.

To "starve" breast cancer cells to achieve treatment

How do cancer cells burn calories? New research from Thomas Jefferson University shows that breast cancer cells rely on different processes to convert fuel into energy. The results were recently published in the Journal of Biochemistry, which also publishes other studies on recombinant rat proteins.

Ubaldo Martinez-Outschoorn, M.D., an assistant professor of medical oncology at Thomas Jefferson University and a researcher at Jefferson's Sidney Kimmel Cancer Center, and his colleagues studied a protein that changes the metabolism of breast cancer cells. Protein TIGAR (an abbreviation of TP53-inducible glycolysis and apoptosis modulators) reduces the ability of cells to convert to sugars through the most common biochemical pathways and to generate energy through glycolysis. It is not clear how this metabolic change alters cancer cells or how cells acquire the energy needed to survive. Through a series of cell and mouse studies, researchers have shown that breast cancer cells with TIGAR proteins that are higher than normal abundance are more invasive and can grow faster than breast cancer cells with normal amounts of TIGAR.

Dr. Martinez-Outschoorn and colleagues showed that when cells express TIGAR, they exchange their metabolic pathways and rely on mitochondria for energy production. Interestingly, high levels of TIGAR produced by cancer cells also alter the metabolism of cells surrounding and maintaining breast cancer and have opposite metabolic effects. TIGARs don't increase their dependence on mitochondrial energy production, but rather make these supporting cells dependent on glycolysis and increased tumor growth. Previous studies have shown that glycolysis in tumors provides energy for cells, making breast cancer more aggressive.

"In fact, 70-80% of breast cancers show a high level of TIGAR, which provides new insights into our study," Dr. Martinez-Outschoorn said. "There are already treatments that block mitochondrial metabolism. We can make use of them to "starve" breast cancer cells."

The two drugs approved for other indications - metformin, antidiabetic therapy and doxycycline, antibiotics - are known to block mitochondrial metabolism. When researchers used these drugs to block TIGAR expression in breast cancer cells, they also blocked mitochondrial metabolism. And they saw a decrease in the aggressiveness of cancer.

"As these drugs have been approved, they have passed human safety tests. And if as our preliminary study shows that they do help to reduce tumor growth in patients, they can be used as a combination therapy with other drugs," said Martinez-Outschoorn.

To this end, Dr. Martinez-Outschoorn is working with Dr. Jennifer Johnson, MD, assistant professor of medical oncology, and Dr. Adam Berger, professor of surgery at Jefferson University, to conduct a clinical trial to test metformin for breast cancer, and women should take doxycycline before surgery. The study will collect and analyze patients' tumors to see if these drugs that inhibit mitochondrial metabolism may have an impact on tumor biology. Flarebio provides you with recombinant proteins of good quality such as recombinant CDH2.

Overweight can lead to abnormal blood flow, resulting in multiple myeloma

A new study from the University of Washington's St. Louis School of Medicine shows that overweight can lead to abnormal blood flow and may lead to multiple myeloma. We know that overweight or obesity increases the risk of multiple myeloma, a plasma cell tumor that occurs in the blood and bone marrow, and that the disease occurs more often after the age of 60. Before the occurrence of multiple myeloma, patients often appear first known as MGUS blood abnormalities. This anomaly refers to that the plasma cells will produce a number of antibody proteins, and this pre-cancerous lesion generally shows no symptoms, so it is difficult to be diagnosed.

"Our study using recombinant human proteins found that obesity can be a risk factor for predicting multiple myeloma," said Dr. Su-Hsin Chang of the University of Washington. "If a patient is diagnosed with MGUS, normal body weight is likely to be a preventable development method of multiple myeloma."

The researchers analyzed data from 7,878 patients (mainly males) who were diagnosed with MGUS between October 1999 and December 2009, and these data were obtained from the American Legionnaire database. Among these subjects, 39.8% were overweight and 33.8% were obese. The researchers followed the group to see if they eventually developed multiple myeloma. Finally, the researchers found that 4.6% of overweight patients (the average follow-up time of about 5.75 years) and 4.3% of obese patients (average follow-up time of about 5.9 years) eventually developed into multiple myeloma, and normal weight patients were only 3.5 %. For multiple myeloma, the results were statistically different. Overweight MGUS patients and obese MGUS patients were 55% and 98% more than normal-weight patients to be likely to develop multiple myeloma.

MGUS patients have elevated levels of antibody M (IgM), while about 3% of people who were more than 50 would show IgM rise, so MGUS is difficult to diagnose and there is no very effective treatment. Multiple myeloma is the third largest blood tumor. According to the American Cancer Society, in 2016, it is expected to have 30330 new patients, and about 12650 patients will die of multiple myeloma.

Dr. Su-Hsin Chang saidm, "According to our findings, overweight and obesity are risk factors for MGUS development into multiple myeloma, and our overweight and obesity are human intervention. We hope that our research results will provide a new strategy for the treatment of our disease. Moreover, we will further study the mechanism of obesity in promoting the development of MGUS to multiple myeloma." Flarebio provides you with good-quality recombinant CDH2 at great prices.

BAG5 protein can save the function of anti-oncoprotein p53

According to research using recombinant dog proteins, among the anti-oncoproteins found so far, p53 is undoubtedly one of the most well-known. It can achieve the curative effect of cancer by affecting cell division, apoptosis, metabolism and other important processes. In nearly half of the tumors, the gene TP53 which expresses this transcription factor show mutations, making p53 lose anti-cancer function. And some functional (GOF) mutations may even make p53 directly "renegade" and promote canceration and tumor resistance.

Mutant p53 is characterized by a greater stability, reflected by being more difficult to be mediated and degradated by ubiquitin ligase MDM2 and CHIP. Interestingly, this stability is limited to cancer cells but not in the normal cells. This allows the mutant p53 to accumulate in the tumor to a high level so as to play its role in promoting cancer. Then, what kind of difference do cancer cells have to make mutant p53 to accumulate at a high level?

Recently, the research team of Prof. Wenwei Hu and Prof. Zhaohui Feng of Rutgers, The State University of New Jersey found that BAG-2-related anti-apoptotic gene (BAG) family proteins BAG5 and BAG2 can prevent pan- Ligase and mutant p53 binding, thereby giving the latter cell-specific stability in the cancer. The results are published in the recent Nature Publishing Group publication Cell Discovery.

In a variety of human breast cancer and lung cancer cell lines and other systems, BAG5 of the five BAG domain can be R175H, R248W or R273H mutant p53 DNA binding domain (DBD) interaction, and BAG5 and wild type P53 between no affinity. At the same time, BAG2, another member of the BAG family, was found to have synergistic effects with BAG5 in enhancing mutant p53 stability. Concomitantly, when BAG5 was overexpressed, the level of mutant p53 was increased in cancer cells, and it decreased when BAG5 was knocked down.

By this interaction, BAG5 prevents MDM2 and CHIP from modifying ubiquitination of mutant p53, thereby ultimately inhibiting degradation of the p53 by the proteasome. Further experiments have shown that BAG5 is essential for the development of functional R248W mutations to play a role in carcinogenesis, including the ability to promote proliferation, proliferation, and drug resistance in cancer cells. It is worth noting that BAG5 is overexpressed in a variety of tumors including breast cancer, skin cancer, colorectal cancer, lung cancer and so on. And the higher the expression level, the worse the prognosis of patients.

BAG family proteins play an important regulatory role in cell division, differentiation and apoptosis, and their common BAG domains have molecular chaperone activity. In this study, BAG5 was found to have proto-oncogenic properties that enhance the ability of cancer cells to proliferate, diffuse and resist drug resistance by increasing the level of functional mutant p53 protein. Therefore, BAG5 has a potential as a therapeutic target for tumors expressing the aforementioned p53 protein. Flarebio provides good-quality recombinant proteins such as recombinant CDH2.