Drinking green tea helps to prevent abdominal aortic aneurysm

Drinking green tea is a habit of many Asians. A recent study by the Journal of Vascular Surgery has shown that drinking green tea can prevent abdominal aortic aneurysm. More related research involving recombinant mouse proteins should be conducted.

Abdominal aortic aneurysm is a disease that occurs in the human aorta, leading to excessive extension and swelling of the arteries. Usually patients show no obvious symptoms of aneurysm, and they usually find the disease when the arteries rupture. If the arterial swelling can be found at an early stage, the doctor usually recommends surgery.

There are many studies confirming that drinking green tea on the human body has many benefits, such as prevention of cancer, cardiovascular disease, inflammation and antioxidant.

"Recent studies have shown that polyphenols existing in green tea can be used to regenerate elastins, which are essential proteins for vascular elasticity," said Shuji Setozaki, MD, and the lead author of the study.

In this study, the investigators used the drug to make the rats suffer from abdominal aortic aneurysms. Researchers have given the green tea polyphenols (the main ingredient in green tea) treated rats to develop a smaller incidence of abdominal aortic aneurysms. These rats have lower levels of inflammation and higher levels of elastin and help to protect the blood vessels from destructive fate. Rats that did not receive green tea polyphenol treatment developed aneurysm, vascular rupture, and 50% of rats died.

"The lifetime of the Japanese is the longest in the world, and studies have shown that 80% of Japanese people have the habit of drinking green tea every day," says Hidetoshi Masumoto, co-author of the study. "We believe that drinking green tea every day should be considered as a new preventive measure to prevent abdominal aortic aneurysms." By the way, Flarebio provides you with good-quality recombinant proteins and antibodies like NES Monoclonal Antibody.

The molecular structure of proteins can be read now

Russian and foreign scientists have learned to read the molecular structure of proteins through the help of X-ray and molecular sulfur atoms, which will accelerate the search for drugs and explore the etiology of rare disease development. Scientists have published the article in the journal Science Advances, which also publishes other studies on recombinant human proteins.

"When I was involved in the first receptor protein structure assay, it took about a year to obtain large-size crystals for classical X-ray diffraction, and we hope that this approach, which is currently being developed, can speed up this work," said Wajim Cherezov from the Moscow Institute of Physics and Technology.

Researchers from the University of Moscow at the University of Moscow and his University of Southern California studied the semi-helical receptor, the GCPR protein. For example, the GCPR protein plays an important role in visual, auditory, and other organ work and transmits signals from the external environment to the cells. Genetic damage associated with its work will lead to serious damage to cell life and cause serious consequences, including blindness.

To this end, scientists are actively studying the protein structure and try to understand their appearance in three-dimensional space. It is very difficult to do this - it is necessary to use astronomical time to calculate its structure on a computer or to separate the protein in pure form to freeze the protein and examine the protein with a strong X-ray laser. Such operations will take a lot of time and effort, which will slow down the GCPR protein research and search for the process of typical damage.

While the Moscow Institute of Physics and some American university scientists can simplify this task. They used free electrons with powerful X-ray lasers and special image processing methods. These images are based on the X-ray reflection and re-radiation patterns of common sulfur atoms in protein molecules.

In this way, Cherezov and his colleagues successfully recovered one of the GCPR proteins with a resolution of 0.25 nm A2A receptor structure and then increased the resolution by 0.19 nm, which is more than twice the diameter of the hydrogen atom. Scientists pointed out that high resolution can not only study the protein structure, but also can see the surrounding fat and water molecules and their interaction with the protein molecules.

Moscow Institute of Physics and Technology said that in the current 800 protein receptors, scientists only know 34 molecular structures. Scientists hope that Cherezov and his colleagues will be able to significantly speed up their research and help to create new and effective drugs for the treatment of large numbers of diseases. Flarebio offers high-quality recombinant proteins and antibodies such as PODXL Monoclonal Antibody.

Sirtuins family and the role of mitochondria in health and disease is well known

With protein entering the people's vision, sirtuins has caused people's attention through its relation with aging and age-related diseases. Sirtuins family and the role of mitochondria in health and disease is well known. Based on a basic survey involving recombinant rat proteins, Marcia Haigis and her Harvard Medical School team presented a profound molecular question: what proteins are associated with sirtuins in cells?

Scientists have created a picture of the interaction of proteins - in mitochondria - found that sirtuins interact with the energy source of cells. Then they used the diagram to reveal how a particular sirtuin works with its protein to keep the cell motivated. Haigis, an associate professor of HMS cell biology, and her colleagues plotted the position of the 89 proteins and observed that the three members of the sirtuin family (SIRT3, SIRT4 and SIRT5) were tightly bound. This approach makes SIRT3 play a key role in regulating the health of mitochondria.

Control of damage is essential for cells and their components. But the researchers demonstrated that SIRT3 intervened in a different way. It responds quickly to mitochondria without compromising yourself. In a paper published by scientists on Cell, a roadmap is provided for future research and shows how they can use it to detect stress responses in mitochondria.

"Knowing how the three mitochondrial sirtuins proteins combine to give us - and this area - really rich information," Haigis said. "The interactive components make us see the stress response. The more we see the more clear that the response is actually regulatory feedback."

Mitochondria must maintain an appropriate concentration gradient on both sides of their inner walls in internal cells, where ATP is the energy source of the cells. When the equilibrium of the membrane potential is destroyed, the pH level rises and the membrane potential sends a signal to destroy the mitochondria. Haigis and her team found that SIRT3 and its binding partner ATP5O changed their markers in the mitochondria by inverting the chemical markers on other proteins, resulting in a response to pH reduction. SIRT3 and ATP50 can label these chemicals - and use energy - to respond to cell pressure until recovery is balanced.

"From a cellular biology point of view, this is a rapid response to stress, which is more effective than mitochondria that are always degraded." Haigis said. Flarebio provides you with good-quality recombinant proteins and antibodies including NES Monoclonal Antibody.

New treatment target of insulin resistance in type 2 diabetes

A team led by researchers at the University of California School of Medicine was able to reverse diabetes insulin resistance and impaired glucose tolerance by eliminating protein galectin-3 (Gal3) in obese diabetic mouse models and using recombinant human proteins.

By binding to the insulin receptor on the cell, Gal3 prevents insulin from binding to the receptor-induced insulin resistance. A team led by Professor Jerrold Olefsky, professor of endocrine and metabolic medicine from the University of California, San Diego School of Medicine, showed that by gene deletion Gal3 or using a drug inhibitor, insulin sensitivity and glucose tolerance can be restored even in older mice normal. However, obese mice remained unchanged.

"This study used Gal3 as a program target for insulin resistance and diabetes in the mouse model," said Olefsky, senior director of the study, a deputy director of scientific research. "Our findings suggest that Gal3 inhibition in the human body may be an effective treatment for diabetes."

Olefsky and other researchers have been studying how chronic tissue inflammation leads to type 2 diabetes insulin resistance. In an article published in a cell journal on November 3, the researchers explained that inflammation needs to disrupt the specific exclusive macrophages of target cells. For example, in obese adipose tissue (fat), 40% of the cells are macrophages. Macrophages also secrete lactose lectin - 3, and then as a signal protein to attract more macrophages, resulting in more Gal3 production.

In addition, the researchers identified the source of bone marrow macrophages that are the source of insulin resistance that leads to insulin resistance. More importantly, the researchers found that Gal3 is secreted by macrophages and can lead to insulin resistance independent of inflammation in the liver, adipocytes and muscle cells.

Gal3 has been linked to other diseases. Olefsky would continue to study Gal3 depletion that may serve as a target for nonalcoholic steatohepatitis and heart and liver fibrosis. By the way, Flarebio offers high-quality recombinant proteins and antibodies such as PODXL Monoclonal Antibody.

Three novel host genes essential for HIV infection through CRISPR gene editing technologies

A study published in Nature Genetics shows that US scientists have identified three novel host genes that are essential for human immunodeficiency virus (HIV) infection through CRISPR / Cas9 gene editing technologies and recombinant human proteins, providing potential treatment target for HIV infection.

On December 19, a research team from the Whitehead Institute, the Broad Institute and the Massachusetts Institute of Technology published a study on Nature and Genetics that using CRISPR / Cas9 to screen for novel host genes that were essential for HIV infection. The lack of these genes will make the host cell resistant to HIV infection, but it will not affect the normal function of cells.

AIDS is a very harmful infectious disease from human immunodeficiency virus (HIV) infection. HIV can attack the body's immune system and greatly damage the immune system, the most important CD4 T lymphocytes, blocking the immune process and leading to the immune system paralysis. Then the body is susceptible to various diseases and malignant tumors, and the mortality is high. The current anti-HIV drug targeting virus protein, because HIV mutation speed is very fast, so it is very easy to show drug-resistant HIV virus. It is difficult to develop HIV-specific vaccine. Therefore, the development of new drugs to target the host genes necessary for HIV infection is a potential method for the treatment of AIDS.

Researchers used CRISPR-Cas9 gene editing technology to establish a T cell bank. In this T cell bank, the researchers targeted more than 18,500 genes based on the CRISPR-Cas9 method, and most of these genes were human protein-coding genes. When these genes were inactivated one after the other, the team used HIV to infect T cells and screened genes that could induce cell resistance to HIV infection and did not affect the normal functioning of cells.

Finally, through a large-scale screening, the research team received a total of five essential HIV genes for HIV infection. The two genes, CD4 and CCR5, were found to be closely related to HIV infection in previous studies. There are three new host genes identified, TPST2 and SLC35B2 are the genes encoding enzyme and can be modified by CCR5 and HIV binding; ALCAM involves in cell adhesion. In subsequent functional trials and experiments in normal T cells, the team found that when CD4-positive T cells were infected with low concentrations of HIV, ALCAM deletion could allow T cells to be immunized against HIV infection. Through the validation of these three genes, the researchers pointed out that these three genes are expected to become a new target for the treatment of HIV infection.

Through the CRISPR-Cas9 gene editing technique, this study screened new host genes that are essential for HIV infection, providing a potential therapeutic target for HIV infection and providing a new direction for the development of new drugs for HIV / AIDS. The researchers believe that this method also applies to the identification of other viral pathogens therapeutic targets. CRISPR / Cas9 gene editing technology has shown great potential in a range of gene therapy applications. We also look forward to early adoption of CRISPR / Cas9 technology to treat AIDS, bringing gospel to AIDS patients! Flarebio offers superior recombinant proteins and antibodies such as NES Monoclonal Antibody for your research.

The small molecule inhibitors of some biogenic enzymes are effective for gliomas

A paper published in the Journal of Cancer Research lists the results of studies on gliomas: 1) identification of biogenic enzymes associated with gliomas; 2) a mechanism for the regulation of such enzymes; 3) by using a mouse model of gliomas, it is shown that the small molecule inhibitors they develop are effective for gliomas. More research involving recombinant rat proteins should be conducted.

Such GA11 inhibitors retain a core structure similar to that of natural inhibitors of biological enzymes; however, such inhibitors have been modified to allow them to pass through the blood-brain barrier.

"In principle, these features make GA11 a candidate for treatment of gliomas," Dr. Ichiro Nakano said.

Nakano is a professor of neurosurgery at the University of Alabama at Birmingham, and he and other researchers are further pre-clinical evaluation of GA11 and its analogues.

"Polymorphic glioblastoma (GBM) is a class of highly lethal tumors. Over the past 30 years, little progress has been made to increase the average survival of patients from five months to 15 to 16 months," Nakano said.

GBM tumors are a class of mixed cell tumors. A small amount of gliomas stem cells induce GBM tumorigenicity, so these stem cells become the primary goal of treatment. Nakano and colleagues infer that determining the regulatory mechanism of bone marrow mesenchymal stem cells activity may develop new and effective treatments. Flarebio offers good-quality recombinant proteins and antibodies like PODXL Monoclonal Antibody.

Anti-Zika virus protein is expected to suppress AIDS

Recently, the Chinese Academy of Medical Sciences Institute of System Medicine, Suzhou Institute of System Medicine (referred to as "the system") has published a research result with the University of California, Los Angeles and other institutions. The researchers found through recombinant human proteins that protein Cholesterol-25-Hydroxylase (CH25H) and its enzymatic reaction product, 25-hydroxycholesterol (25HC), had a definitive protective effect on the disease caused by Zika virus infection and was expected to inhibit Ebola Viruses, HIV and so on. The results have been published by the internationally renowned journal Immunity.

Zika virus broke out in Brazil and other countries in the United States from 2015 and is still a global threat to human health. China has also reported dozens of cases of imported Zika cases. Once pregnant women infected with Zika virus, it may lead to fetal development abnormalities, neonatal head disease and other neurological diseases. There is currently no effective therapy for the Zika virus, nor through the clinical trial of the vaccine.

According to Dr. Li Chunfeng, who participated in the research system, as early as in 2013, Chinese and American scientists discovered the broad-spectrum antiviral effect of 25-hydroxycholesterol. After the outbreak of the Zika virus, the system responded to the national call and the Institute of Microbiology and Epidemiology of the Academy of Military Medical Sciences, Chinese Academy of Sciences Institute of Genetics and Development and the University of California, Los Angeles and other institutions carried out joint research on the cholesterol-25-hydroxy.

Cholesterol-25-hydroxylase is an interferon-stimulating gene whose gene expression product allows the cholesterol to be oxidized to produce 25-hydroxycholesterol. Through the experiment, the researchers found that 25-hydroxy cholesterol can directly block the virus into the cell process, including a variety of insect vector yellow viruses have a broad spectrum of antiviral activity including Zika virus. Researchers used the mouse model of the Zika virus infection and rhesus animal model and found that 25-hydroxy cholesterol treatment can significantly inhibit the virus in vivo replication and can effectively prevent the occurrence of microcephaly.

Professor Cheng Genhong, who participated in the study, said that 25-hydroxycholesterol was the first small molecule to be found in the monkey to inhibit the replication of the Zika virus and was the first compound to prevent the microcephaly caused by infection of the virus.

"Theoretically, it may have the same effect on the human body. Our next step is to begin clinical trials to verify the effectiveness of 25-hydroxy cholesterol on the human body," Cheng Genhong said. The system will also examine the antiviral effect of 25-hydroxycholesterol derivatives and look for substances that are more effective in suppressing Zika virus infection.

In addition, based on 25-hydroxy-cholesterol broad-spectrum antiviral effect, Chinese and American scientists have experimentally confirmed that 25-hydroxy cholesterol can inhibit Ebola virus, AIDS and so on. The two sides will continue to cooperate to apply it to the prevention and treatment of new viral diseases, which will provide new programs for effective prevention and treatment of viral infectious diseases. Flarebio provides you with good-quality recombinant proteins and antibodies such NES Monoclonal Antibody.

The early diagnosis method of Parkinson's disease

Parkinson's disease has no specific symptoms and thus is difficult to be diagnosed in time. When patients with mobility disorders can be diagnosed, the nerve cells have got irreversible damage, and the effect of drug treatment is quite limited. Researchers at the University of Würzburg and the University of Fort Worth have made significant progress in this research through recombinant mouse proteins and have succeeded in discovering that the risk of Parkinson's disease can be diagnosed by skin tests, which is earlier than the current diagnosis.

Scientists have examined the skin of patients without Parkinson's symptoms and found α-synuclein specific to Parkinson's patients in their nerve endings. This protein, which is characteristic of Parkinson's disease, is no stranger to the industry, but it is often determined in the patient's brain only after the patient has died.

Now the German scientists in the patient before the onset or in the early sick through a small five-mm skin biopsy can diagnose Parkinson's disease, so that the nerve can be destroyed before the patient can be targeted and effective treatment. By the way, Flarebio provides you with high-quality recombinant proteins and antibodies like recombinant TLR2.

The fatal weakness of leukemia has been discovered

Scientists have discovered two kinds of signaling proteins that make cancer cells resistant to chemotherapy, and according to studies on recombinant human proteins, they can eliminate leukemia by blocking these signal proteins.

The findings are published in Nature Medicine, and researchers at the Cincinnati Children's Hospital Medical Center have shown that blocking the combination of signal protein c-Fos and Dusp1 may cure a variety of kinase-driven, refractory leukemia and solid Cancer, including acute myeloid leukemia (AML), lung cancer, breast cancer and chronic myeloid leukemia (CML).

"We believe that our data will change the way we think about cancer development and targeted care over the next five years," the researchers said. "This study identifies the potential weakness of the kinase to drive cancer, and we suggest that it is cured and not treated."

After identifying c-Fos and Dusp1, the researchers used a combination therapy approach. Treatment combinations include: 1. Personal therapy with tyrosine kinase inhibitors, imatinib; 2. Single inhibitor treatment of c-Fos Dusp1; 3. Imatinib treatment of two molecular inhibitors c-Fos Dusp1 binding treatment. The results of the study showed that after a month of treatment, 90% of the mice were treated with imatinib in combination with two molecular inhibitors, and there were no signs of residual disease. In addition, the researchers also found that the use of a single inhibitor can also eradicate the disease in mice.

Before the clinical trial, the researchers also need to repeatedly verify that they will continue to track the test c-Fos and Dusp1 on the kinase-driven effects of various types of cancer. Flarebio provides you with superior recombinant proteins like recombinant ECEL1 at competitive prices.

To produce new proteins to achieve a variety of magical functions

Protein structure almost has unlimited possibilities. According to our needs to design and manufacture of proteins, it is possible to achieve a variety of magical functions through a lot of recombinant mouse proteins.

Protein is the "labor" of all living creatures, carrying out various orders from DNA. It also has a variety of complex structures to achieve all the important functions of humans and all organisms, including digestive food, tissue growth, blood oxygen transmission, cell division, neuronal activation, muscle supply and so on. Surprisingly, the function of such a diversity of proteins comes only from the combined sequence of 20 amino acid molecules in the region. Until now, the researchers have just begun to understand how these linetypes are folded into complex structures.

Even more surprising is that nature seems to use only a small part of all possible protein structures, although the latter is large in number. Therefore, the use of existing amino acid design with a special structure of the unconventional protein, that is, nature has never had synthetic protein, having a very attractive application prospects. Synthetic protein method is: to genetic transform bacteria to make its DNA control produce a specific amino acid sequence and then synthesize proteins. It is important to be able to produce and study synthetic proteins at the atomic level for the development of new areas of basic research and for practical applications in more areas.

At the beginning of the design process, supposing a new protein structure that resolves a particular problem or implements a function, and then in turn determines a candidate amino acid sequence that can be folded into such a structure. The Roseetta protein model design software identifies the most promising candidates: the amino acid sequence that folds the lowest energy state of the target structure. Next, these sequences are transferred from the computer to the laboratory, producing synthetic proteins and testing.

At present, there is no technology comparable to the wonderful function of protein implementation. The infinite possibilities of synthetic proteins allow protein design to greatly expand the ability of protein technology. Flarebio offers high-quality recombinant proteins such as recombinant ITGB5 at competitive prices.

New research has demonstrated the possibility of HIV vaccines

The Duke Health Group described the development pathways for HIV-protected antibodies as well as synthetic viruses that mimic the HIV surface structure and it induces HIV antibodies through vaccines. At present, the purpose of the HIV vaccine is to extensively induce neutralizing antibodies, one of which is to develop part of the antibody that can recognize the HIV surface structure, and our research through recombinant rat proteins demonstrates this possibility.

Researchers have found that the immune system of the infected people responds to the virus through the cooperation efforts between the b cell lineages, thus GF-induced neutralizing antibodies. The antibody development process involves a rare activity of the genetically-modified protective antibody.

Immunogen imitates and neutralizes antibodies and immune attacks in the exact location, and synthetic immunogen can find this exact location. In the process of testing primates, synthesis of immunogen can induce antibodies into this critical area.

"We have found weaknesses in the surface structure of HIV, and not just a place but a few. Thus, the effective vaccine can target at least one weakness so that the immune system is armed to deal with the mutation which is going to happen," the researchers said.

The complete study was published in the journal Science Translational Medicine. Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. We provide good-quality recombinant proteins like recombinant COLEC12 at competitive prices.

Cancer cells may spread faster due to fat metabolism

Hepatocarcinoma is the third leading cause of cancer-related death worldwide and is the fastest growing cancer in Australia. "Many people suspect that the fatal nature of liver cancer is the process of cell metabolism, which is thought to play an important role in helping cancer cells to proliferate," says Kyle Hoehn, associate professor at UNSW. The team led by Hoehn managed to successfully prevent the formation of fat in hepatocytes of transgenic mice with unintended consequences. Unlike the team predicted that the termination of the growth of cancer cells, blocking this metabolic pathway led to more than twice the emergence of the tumor. The surprising results were published this week in Nature Communications, which also publishes other studies on recombinant human proteins.

Hoehn said, "It is currently developing drugs to target and block this metabolic pathway, which is considered promising to treat the liver and other cancers. These results may cause some concern at least for liver cancer. Our findings are completely contrary to intuition. But it is clear that any use of these drugs in the treatment of liver cancer should be more cautious in the future because there may be unintended consequences."

When cells divide, they need to reconstruct all of their structural components including their protective film made of fat and promote the process through lipid production. "The fat generation is the hallmark of invasive liver cancer, and the survival rate of high-fat-producing tumors is the lowest," Hoehn said. "Before we start this experiment, we believe that if you can knock out fat-producing legs, then you can stop rapid formation or proliferation of cancer cells."

The team tested whether their genetically-modified mice could obtain cancer by exposure to DNA-damaging carcinogens and introducing high-fat diets. These injuries increase the risk of developing advanced tumors of life. At 9 months of age, they compared the tumor burden of genetically-modified mice and mice with normal liver fat production. The results were very surprising. In addition, the team found that cancer cells rapidly adapt to the loss of fat production: they began to remove more fat from the blood and burn more fat by burning less fat. Thus, by pulling out one leg of lipid metabolism, they got stronger.

Although it looks like a retrograde on the surface of cancer treatment, Hoehn said, "Cancer cells seem to always have a solution. They are smart little bastards. This finding has revealed valuable insights into the complex biology of cancer cells and also identifies possible new targets for future drugs: mechanisms that drive antioxidant defense systems or fat intake." By the way, Flarebio offers high-quality recombinant proteins such as recombinant NPP1 for your research.

Researchers conduct research new treatment of cancer stem cells

Many cancer patients enter the remission after chemotherapy, but they will continue to relapse after the treatment. More and more evidence suggests that this is due to the infinite reproduction of cancer stem cells may grow new tumors. A team from Milan, Italy, designed a program specifically targeted to cancer stem cells in certain cancers and reduced their tumorigenic potential. The study was published in the EMBO Molecular Medicine, which has published many studies on various recombinant proteins like recombinant rat proteins.

Each of our bodies has stem cells that are constantly splitting and renewing cells in the body. The team led by Pier Paolo Di Fiore and Salvatore Pece explored the role of Numb protein in maintaining stem cells in normal mammary gland development and found that Numb protein is necessary to maintain balance before stem cell and gland differentiation. Numb upregulates p53, a protein that blocks cell division. When Numb is deleted, p53 is also reduced, leading to increased self-replication of stem cells, which may lead to tumor formation.

In many breast cancers, Numb concentrations are lower, which is associated with poor prognosis. In this study, the role of Numb in these tumors was observed and found to be deficient in Numb's tumors, and the number of cancer stem cells increased, thus providing higher proliferation and growth potential for tumors. In addition, the researchers found that p53 plays an important role in it. When the concentration of Numb decreases, the concentration of p53 will also decrease. However, when p53 levels are recovered by blocking the degradation of Nutlin-3, the tumor is less aggressive and has fewer cancer stem cells. Many drugs targeting p53 pathways, such as Nutlin-3, are currently in clinical development.

Finally, the researchers examined the potential for the combination of Nutlin-3 and paclitaxel (a common chemotherapeutic agent). Although paclitaxel alone can reduce the tumor, the risk of recurrence is great once terminating the treatment. The combination of paclitaxel and Nutlin-3 not only enhances the response of paclitaxel to tumors, but also prevents Numb-deficient tumors from proliferating after treatment has ceased. This indicates that Nutlin-3 or similar drugs have the potential to fight against chemical resistance caused by cancer stem cells.

In the context of current research, researchers have developed preclinical model systems that specifically capture the effects on cancer stem cell therapy. All results were based on transplanting the patient's tumor cells into mice and then studying the presence of stem cells or the invasive nature of the cancer by a variety of methods. The system of testing different effects of different compounds on cancer stem cells may be a valuable tool in future experiments.

These preclinical findings suggest that patients with breast cancer with a defective expression of Numb may be eligible for the use of the currently clinically developed Nutlin-3 similar drugs. Using the same preclinical model, researchers are testing the efficacy of this candidate drug for cancer stem cells, as well as the possibility of minimal toxicity of standard chemotherapy regimens in the treatment of human breast cancer. By the way, Flarebio provides you with high-quality recombinant proteins such as recombinant ITGB2 at good prices.

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.

Researchers have found the key protein of leukemia

According to studies on recombinant mouse proteins, scientists have found that regulatory protein ENL can promote the occurrence of leukemia. This has deepened the academic understanding of transcriptional regulation and suggests a potential leukemia therapy.

The cause of blood tumors is usually chromosome translocation, resulting in two proteins connected to the formation of fusion protein, and ultimately causing disease. Recombinant protein in regulatory protein mixed lineage leukemia (MLL) is also commonly found in invasive childhood leukemia and is associated with poor prognosis. Therefore, it is necessary to develop a leukemia treatment strategy based on MLL rearranged (MLL-r) fusion protein. In the journal Nature, Erb et al. and He et al., point out that ENL protein is a key factor in the survival of MLL-r cells in leukemia. Erb et al. and Wan et al. have shown that this "read" ability of ENL to acetylated histones is critical to induction of MLL-r leukemia.

Erb et al. and Wan et al. found another complementary mechanism for SEC and DotCom stability. They found that the inactivation of ENL weakened the function of SEC and DotCom in MLL-r cells. The ability of ENL to bind to SEC and DotCom suggests a model that recognizes the acetylated H3 through the YEATS domain, enhancing the stability of the SEC and DotCom complexes with DNA binding and regulating the activity of the genomic abnormalities.

Protein ENL is essential for MLL-r leukemia. Some leukemias are found in some of the MLL protein and another part of the protein mixture of protein. The second protein is usually part of the SEC (super elongation complex) protein complex or the DotCom (DOT1L-containing complex). Both of these protein complexes regulate gene transcription procedures in MLL-r leukemia (complete and partially fused SEC / DotCom complexes). The ENL protein binds to two complexes, while the complex is fused to the MLL in the cell. ENL interacts with the fused SEC / DotCom and interacts with the fused SEC / DotCom. ENL contains a YEATS domain that recognizes a specific acetyl (Ac) on histone H3. Erb et al. and Wan et al. demonstrated that the YEATS domain of the ENL protein helps to stabilize the binding of SEC and DotCom to DNA and promote gene expression that drives leukemia.

This new model suggests a possibility that drugs such as small molecule inhibitors targeting the ENL YEATS domain can selectively kill leukemia MLL-r cells. Other cell types appear to be able to tolerate ENL loss to a large extent, but the SEC, DotCom and ENL are expressed in a variety of cells, so it is important to understand this tolerance when developing such drugs on the difference.

The effect of these combination therapies suggests that multiple histone-modified signals act together to form a specific epigenetic state of MLL-r leukemia. Thus, long-targeted therapy is more effective and can reduce the emergence of drug resistance - which is one of the risks of single drug therapy. Thus, Erb et al. and Wan et al.'s findings on ENL not only deepen our understanding of how cells integrate transcription-related signals, but also provide new insights into the treatment of complex diseases. By the way, Flarebio offers high-quality recombinant proteins like recombinant ECE1 at competitive prices.

To study new cancer substitutive therapies of cancer targeted at protein moesin

In an online article published in Journal of Clinical Research at the University of South Carolina Medical University (MUSC) on March 13, 2017, the researchers reported preclinical studies showing that the membrane domain of tissue protein moesin controls the function of regulatory T cells (Treg) and the abundance and stability of transforming growth factor-β (TGF-β) receptors on the cell surface, providing potential therapeutic targets for cancer immunotherapy. Even so, more research involving recombinant human proteins should be conducted.

Their results show that TGF- β acts at the protein level to produce Treg in the tumor microenvironment. Although the human immune system is capable of eradicating cancer, Treg inhibits immune responses and protects cancer cells from tumor cytotoxicity (i.e., cytotoxic) and T cells effect.

When T cells, leukocyte subtypes, effectively attack and kill tumor cells, the protein TGF- β is activated. However, the immune system has a complex check and balance network to ensure that the body does not produce so much toxic T cells that it hurts its own cells and tissues. Inhibition of moesin can help to prevent natural T cells from converting to Treg, thereby restoring an antitumor immune response.

"Because moesin supports more Treg production, we can design moesin inhibitors to stop or slow the activity of TGF-β signaling and slow down Treg transformation so that antitumor T cells can have the opportunity to see cancer and eradicate it," said Zihai Li, a senior author of this article, MUSC microbes Director of the Department of Immunology and Immunology.

Perhaps the most notable outcome is the study of melanoma mouse models involving the treatment of adoptive T cells. In adoptive T cell therapy, tumor killer T cells are harvested from people or animals suffering from cancer and amplified or otherwise "sensitized" before being reintroduced into the donor. Although these regressive cells can kill tumors very effectively, they do not always survive for long periods of time.

The MUSC team showed that these re-cultured anti-cancer CD8 + T cells were not only activated and expanded rapidly in mice lacking moesin, but they also survived for a longer period of time and reduced the likelihood of recurrence. In fact, after the transfer of adoptive T cells, all mice with moesin were recurrent, and most mice lacking moesin were cured.

These findings suggest that moesin may be the development of new therapeutic targets for the treatment of cancer and Treg-related immune diseases. Moesin's chemotherapeutic agents can control the function of T cells by inhibiting moesin in cancer or inducing its treatment of autoimmune diseases. Moesin modulators can also be combined with current immunotherapy regimens. These findings are of great significance to the field and provide many directions for further research on alternative therapies. Flarebio offers recombinant proteins of good quality such as recombinant CDH15 at competitive prices.

This protein is identified to influence healthy immune system

Researchers have found through recombinant dog proteins that protein Myb plays a vital role in maintaining the health of our immune system and preventing the development of immune and inflammatory diseases. Preclinical studies have shown that Myb gives immune cells known as regulatory T (Treg) cells "authority" to control the intensity of immune responses. The study was published on Immunity and was led by Dr. Shelia Dias and Professor Stephen Nutt in collaboration with immunologists and bioinformatics teams at the Walter and Eliza Hall Institutes.

Dr. Dias said it was the first sign that Myb had an impact on the immune system. "For decades, Myb has been associated with the formation of multiple types of cancer," Dr. Dias said. "Our study shows that Myb is also important for the function of Treg cells, and we find that at the site where Myb is absent, the ability of Treg cells controlling immune response is also weak, and the immune system continues to respond to a range of threats from mild infections to life-threatening disease. Researchers around the world are investigating how the immune system coordinates and controls health."

"There are many different cell types in the immune system, each with a specific obligation. And when these cells fail to perform their duties, there is a risk of health," Dr. Dias said.

Professor Nutt said, "Increasing the knowledge of the mechanisms that control the immune response is critical to understand how immunization and inflammatory illness occurs and to ultimately develop more effective treatment. If we can figure out how Myb affects Treg cells in the immune system, we may be able to manipulate this activity."

"In the long run, we would like to extend this study to the clinic in order to understand whether our findings can be applied to human immunology," he said. Flarebio provides you with recombinant proteins of good quality including recombinant TLR2.

To change the direction of treatment of Alzheimer's disease

Researchers at the University of Lund, Sweden, used the latest technology to generate the formation of toxic clumps prior to β-amyloid. According to previous studies on recombinant rat proteins, β-amyloid is the root of Alzheimer's disease.

The scientific community has long believed that β-amyloid plaques are instantaneously present, and therefore the term "popcorn plaques" comes from it. However, the infrared spectrum shows the result is not the case.

"No one has used this method to observe the development of Alzheimer's disease," says Gunnar Gouras, professor of experimental neurology at Lund University. "These images tell us that progress in β-amyloid is slower than we thought and that Alzheimer's disease has a new understanding of the development process."

What does this discovery herald? Researchers use biochemical identification to see closer to Alzheimer's disease early brain changes. The results reveal another finding that β-amyloid is not a single peptide, which is linked together by four peptide units and exhibits a tetrameric form.

This finding provides a new hypothesis for the treatment of the disease - the abnormal separation of these four peptides may be the beginning of the accumulation of β -amyloid, followed by the formation of plaques. Another amyloid disease is associated with transthyretin amyloidosis, and tetrameric decomposition has been identified as the key to the development of the disease. For this disease, there is already a drug that stabilizes the tetramer, thereby stabilizing the β -amyloid protein for therapeutic purposes.

Thus, the finding can change the direction of our treatment of Alzheimer's disease. Most of the drugs are currently designed to eliminate plaques. Flarebio offers high-quality recombinant proteins like recombinant TLR2 at competitive prices.

Scientists have developed new method of cancer immunotherapy

A new generation of cancer immunotherapy has been successful, and this therapy acts on the adaptive immune system, that is, foreign and diseased cells to accurately attack the specialized cells. The other arm of the immune system, known as innate immunity, is not idle in this battle. More research involving in recombinant dog proteins should be conducted.

In a new study in the journal Nature, scientists at the Dana-Farber Cancer Institute report that compounds that can reverse innate immune system cells - transforming them from tumor promoters into tumor antagonists - cause breast cancer in mice to contract withdrawal transfer. When combined with chemotherapy or another immunotherapy, the new compound significantly prolongs the tumor remission. The authors suggest that these findings suggest a way to make a complete composition of the immune system affecting human cancer.

"Most of the current forms of cancer immunotherapy are "taught" by attacking tumor cells or eliminating the barriers to such attacks, affecting the behavior of T cells - leukocytes are part of the adaptive immune system," Guerriero said. "This strategy has been effective against several types of cancer, but usually only a fraction of patients benefit. We hope to see the use of the immune system to produce better results.

The newly-studied target is innate immune system cells called tumor-associated macrophages (TAM). They are usually deeply embedded in the tumor, but they are part of the immune system - the body against the disease defense system - they often promote tumor growth. In this way, they respond to the clues of the tumor itself.

The role of macrophages - both protective and destructive - depends on signals from their environment. In wound healing, for example, macrophages regulate the components of the immune system, removing damaged tissues and restoring affected areas. Tumor macrophages try to hijack these.

In previous studies, scientists from Dana-Farber and colleagues showed that a compound called TMP195 could transform TAMs from helping tumor growth to attacking them. TMP195 converts macrophage responses by altering the genetic activity within TAMs.

In this study, TMP195 significantly reduced the rate of tumor growth in breast cancer mice. They followed the combination of TMP195 with various chemotherapy regimens and an immunotherapy form called T cell checkpoint blockade. In both cases, the combination produces a longer remission of breast cancer than the TMP195 alone. Flarebio provides you with superior recombinant proteins including recombinant Itgb5.

To study action mechanism of transport proteins ABCB1 and ABCG2

How is the resistance of cancer cells affected by ABC-transporter? A related new study paper through recombinant mouse proteins has been published in the open access journal BioDiscovery, studying the second generation tyrosine kinase inhibitor (TKI) - dasatinib (DAS) and ATP binding (ABC) transport proteins ABCB1 and ABCG2 mechanism to assess whether these drug transporters may impair the therapeutic effect.

The "targeted" treatment of cancer is an effective way to minimize the damage to healthy cells. Targeted therapy has revolutionized cancer treatment in the past few decades through the use of reasonably designed drugs that interfere with the specific molecules (molecular targets) necessary for the proliferation and survival of malignant cells.

Although DAS is an excellent choice for the treatment of chronic myeloid leukemia resistant to imatinib, recent laboratory studies have shown that the antiproliferative effect of DAS can be significantly reduced when ATP binds to ABC transporters, ABCB1 and ABCG2.

"Although this relationship is important, we still don't know whether these drug transporters will damage DAS's clinical treatment," explains Dr. Petr Mlejnek, Ph.D., Olomouc, University of Palacky, Czech Republic. "We believe that the expression level of drug transporters is a key factor in the outcome and may therefore help explain the existing controversy. We decided to study the relationship between ABCB1 and ABCG2 expression levels and in vitro resistance to DAS.

In their study, Dr. Petr Mlejnek from the University of Olomouc Palacky, Czech Republic, and his team observed that the expression level of ABC-transporters studied was an important factor influencing cell resistance. Although the anti-proliferative and pro-apoptotic effects of DAS can be reduced by ABCB1 or ABCG2 at clinically relevant concentrations, the actual effect of ABC transporters on DAS efficiency depends on their expression levels. The lower expression level of ABC transporters mediates lower resistance. Considering the fact that the expression levels of ABCB1 and ABCG2 transporters are almost not high in clinical samples, their contribution to overall resistance to DAS is significant. Flarebio offers high-quality recombinant proteins such as recombinant ECEL1 at good prices.

Researchers have identified the gene which affecting brain tumor development

Researchers at Cedars-Sinai have identified a stem cell regulatory gene that affects the growth of brain tumors and it can strongly affect patient survival. The findings involving recombinant human proteins are published in the online version of Scientific Reports, which will allow physicians to get closer to the goal: to better predict the prognosis of brain tumor patients and to develop more personalized treatments for them.

In order to enhance the understanding of how glioma stem cells (GCSCs) reproduce and how they affect patient survival, the researchers spent three years analyzing the genetic composition of more than 4,000 brain tumors. During their investigation, they identified genes that regulate tumor growth, and the gene is called ZEB1. Researchers' analysis showed that patients with brain cancer without this gene often had a lower survival rate.

"The cancer in patients who do not have this gene in the tumor is more aggressive and develops into an uncontrollable number of cell types," said Dr. John Yu, associate professor of neurosurgery oncology and deputy director of the Department of Neurosurgery. These new information can help us measure mutations in these patients so that we can provide more accurate prognosis and treatment plans.

When cancer cells (also known as malignant cells) appear in the brain tissue, brain cancer happens. This year, more than 23,000 people will suffer from primary cancerous tumor of brain. According to the National Cancer Institute and the American Cancer Society, about 16,000 of these patients will die.

Yu and colleagues have pointed out that although some brain cancer patients are born without this gene and others have, the gene has become less powerful over time - it may have a pathogenic effect.

"Compared with those with the gene, we found that the survival time was reduced by eight and a half months in patients with mild glioma with ZEB1 gene mutations," said Yu, co-chair of Cedars-Sinai Surgical Neuroinology. "We know that chemotherapy in some people with gene loss is ineffective, so we have to treat them with different drugs." Flarebio provides you with good-quality recombinant proteins including recombinant Nrg2 at competitive prices.

A study which explains chemotherapy drug resistance

The article published in the EMBO journal states that scientists have discovered a specific protein associated with drug resistance that could lead to new chemotherapy tools. Researchers have pointed out the role of f FOXO1 in chemotherapeutic resistance. In addition, through recombinant mouse proteins, they have identified a potential chemotherapy tool that is, constructing a short segment of amino acids: peptides.

There are many forms of cancer drugs. Among them, taxane chemicals are used for the treatment of advanced cancer. However, as time goes by, the taxane becomes less effective. Cancer cells communicate through other pathways. In this study, the researchers focused on how cancer cells develop other pathways and how to produce drug resistance.

Cells need energy functions. Kinases help chemicals react back and forth in specific molecules, usually in proteins. This activity will burn cell function. The scientists studied the serine / threonine kinase AKT. AKT helps cells survive, playing a very important role in many kinds of cancer. It can close the AKT drugs to improve the effectiveness of chemotherapy. However, due to the inherent complexity of cell communication, this therapy itself may allow tumor survival.

In this study, scientists used taxanes on cancer cells to block or inhibit AKT action, and they found that taxanes prevented FOXO1 protein from migrating cells to the nucleus. FOXO1 stays in the nucleus. In another protein, it becomes signal of active and improperly begins, helping cancer survive and produce drug resistance. "This is why AKT inhibitors are not approved by clinical trials. However, when FOXO1 migrates out of the nucleus, it binds to a protein called IQGAP1 scaffold. Binding action will prevent chemotherapy resistance. "We also found that the combination of taxane and FOXO1-derived inhibitors can inhibit cancer growth." By the way, Flarebio offers high-quality recombinant proteins like recombinant COLEC12 for your research.

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 discovered more in the processes of protein folding

Biophysicists at the JILA Physics Research Center at the University of Colorado, USA, have more surprisingly measured the folding of proteins and are surprised to find that their folding processes are more complex than scientists have predicted. This means that our understanding on the degree of protein is still in the fur. Protein response is far more sophisticated than we have detected in the past 17 years. Thus, more research involved in recombinant mouse proteins should be done.

The basic composition of protein molecules is the amino acid chain. Through a series of intermediate processes, like the origami, the amino acid chain is folded into a three-dimensional structure, and then having a function. Accurately describing this folding process requires the formation of all intermediate states. The latest research reveals many unknown states in the process, and the results are published in the March 3 issue of the journal Science.

Researchers are researching a membrane protein that converts light into chemical energy, called bacteriorhodopsin (BR), with a molecular weight of about 26 kD. It provides a model for cell membrane receptor proteins and also contributes to elucidating the mechanism of interaction between the receptor and the signal in the signal transduction pathway of the human body, the BR or the proton protein of the ionomer channel on the cell membrane, and the role of the proton transfer membrane, so that it can be the other ion channel protein. Finally, its photoelectric response and photochromic specific make it have broad prospects in the solar cell, artificial retina, optical information storage, neural networks, bio-chip and other fields. Therefore, BR research has attracted the attention of countless scientists in the world. However, the folding of membrane proteins is more difficult than the folding of globular proteins with relatively small size.

Tom Perkins and colleagues who led the study used the nano-scale atomic force microscope (AFM) to stretch the BR protein and measure its degree of stretch at different stretching rates (nanometers per second). The measurement method comes from JILA's previous study, a soft AFM short probe (short, soft AFM) that can quickly measure the sudden change in force during protein development and immediately feed back a signal in the middle of the protein. By further refining these AFM probes, JILA researchers can detect BR proteins at different pull rates faster (faster than 100 times) and more accurate (10 times higher accuracy).

The JILA team found that the intermediate state was not only more than expected, and that the entire folding process was only 8 microseconds (1 microsecond equal to one millionth of a second). The results explain why there is a long-standing difference between experimental data and molecular simulations. At the same time, for the molecular simulation means to provide confidence in the future study of membrane protein behavior identified a path.

The technology can also be applied to many other molecular studies such as medical, protein, and drug interactions. More specific examples, such as structural and functional studies of proteins that are similar to BR structures are associated with many human diseases and drugs. By the way, Flarebio provides you with superior recombinant proteins such as recombinant ECE1 at competitive prices.

REV-ERB can reduce LDL (LDL) cholesterol in animal models

A paper published in Biochemical Pharmacology by researchers at Saint Louis University have studied through recombinant human proteins about how nuclear receptors called REV-ERB are involved in the regulation of cholesterol metabolism. Their findings suggest that drugs targeting such nuclear receptors may be able to reduce LDL (LDL) cholesterol in animal models.

Dr. Thomas Burris, Ph.D., director of pharmacology and physiology at the University of St. Louis, said that studying the nuclear receptor signaling, the intracellular information system is the basis of many physiological processes used by the body. He identifies the natural hormones that regulate the nuclear receptors, and then synthesizes the compounds to target these receptors to develop drugs that treat the disease. REV-ERB is a nuclear receptor, a protein that plays a variety of roles. In the past, Burris has studied its role in regulating the internal clock of mammals.

Cholesterol is an essential component of the cell membrane. Atherosclerosis, plaque accumulation in the arteries, is caused by cholesterol metabolism disorders. Drugs such as statins can reduce low-density lipoprotein (LDL) cholesterol levels and atherosclerosis risk, but they are not suitable for everyone. Some patients stop medication because of side effects. Thus, additional cholesterol-lowering drugs are required. Nuclear receptors regulate basic physiological processes such as growth, development and metabolic balance in vivo. REV-ERB is a nuclear receptor that binds to a particular DNA sequence and limits the transcription of the target gene. Studies over the past decade have shown that REV-ERB plays an important role in metabolic pathways. Previous data indicate that REV-ERB lacks lipid metabolism that results in destruction; mice lacking REV-ERB expression show a significant increase in LDL and total cholesterol.

Similarly, in the previous study, Burris found a recombinant version of SR9009 called REV-ERB to reduce cytoplasmic cholesterol and triglyceride levels in animal models. In this study, Burris found that REV-ERB worked in the inhibition of several cholesterol-related enzyme genes and that pharmacological activation of REV-ERB resulted in further inhibition of these genes, which was associated with reduced cholesterol levels. These results reveal the way REV-ERB directly and indirectly regulates cholesterol and indicates that targeted REV-ERB may be an effective method for clinically suppressing LDL cholesterol levels. Flarebio offers high-quality recombinant proteins like recombinant CDH15.

Certain types of immune cells in tumors may increase survival

A pilot study using recombinant rat proteins and conducted by researchers at the University of Otago shows that patients with colorectal cancer having certain types of immune cells in their tumors may increase their survival. Researchers at the Department of Microbiology and Immunology have found that people with more "T-regulated" immune cells in colorectal tumors are more likely to be disease-free and have a longer life span than those with fewer of these cells.

The study involved 32 patients with earl-stage (II) colorectal cancer. These patients received more than 5 years of follow-up: 13 patients showed cancer recurrence during this period; 19 patients showed no recurrence. These findings have been published in the International Journal Cancer Immunology, Immunotherapy.

By making use of a new tool to detect tumor and immune cells in immune cells infiltrates and measuring more complex immune cells, researchers investigated which type of immune response is associated with patient survival. The researchers found that although Immunoscore was superior to the current staging in assessing patient survival, the addition of "effectally Treg" immune cells made it better to survive. Kirsten Ward-Hartstonge, co-author and doctoral scholar of the study, said, " The findings suggest that it is possible to detect the immune response of patients with colorectal cancer to estimate which patients may be suffering from cancer and therefore should be given additional treatment. This information can be used to customize existing treatment programs to target people who really need them, rather than taking more blankets."

"About a quarter of patients who are currently considered ‘low risk’ will use the current staging method to potentially develop the disease again," Miss Ward-Hartstonge said. These patients usually do not receive chemotherapy or radiotherapy because the risks and costs are considered to be more beneficial.

By detecting immune cells from individual patients and "Treg" immune cells, it may be possible to more accurately identify patients with high risk and more effective treatment. Other studies have shown that New Zealand and Australia have the highest incidence and mortality rates for colorectal cancer in the world. It is possible to more accurately identify patients with high risk and more effective treatment. Other studies have shown that New Zealand and Australia have the highest incidence and mortality rates for colorectal cancer in the world. Flarebio offers high-quality recombinant proteins of good quality such as recombinant TLR2 at good prices.

To prevent and treat liver metabolism in new method

Recently, the Nature - Medicine published the latest research results by Professor Li Hongliang research team at the Wuhan University School of Basic Medical Dean online, revealing through recombinant dog proteins for the first time that the natural immune important molecules CFLAR plays key negative regulatory role in nonalcoholic steatohepatitis (NASH) disease, further clarifying its molecular mechanism and having important clinical significance on NASH prevention and treatment.

This study is another major breakthrough in the field of liver metabolic disease research, and it provides a new insight into the understanding of the pathogenesis of NASH, which lays a theoretical foundation for the development of targeted therapy. Professor Li Hongliang told reporters, "CFLAR is an important molecule of the natural immune regulation network. After eight years of research and based on a variety of genetic engineering animal disease model and molecular biology, the team confirmed the key inhibition role of CFLAR on NASH Inflammation, fibrosis, insulin resistance and liver lipid accumulation.

Further in-depth molecular mechanism studies have shown that CFLAR improves and reverses NASH progression by inhibiting the formation of N-dimerization of ASK1 and blocking ASK1 activation. By the way, Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. It offers good-quality recombinant proteins like recombinant Aoc3 for your research at reasonable prices.

Researchers have found the key to molecular aging in the blood and immune systems

The team at the new University of California, San Francisco has found the key to molecular aging in the blood and immune systems, and it is expected to address chronic diseases, anemia, blood cancer and various diseases caused by infection. The study has been published in the journal Nature, which also publishes other studies on recombinant rat proteins.

The researchers said, "In addition to the normal cell waste disposal, the autophagy has influences on the orderly maintenance of hematopoietic stem cells (hsc), as well as the whole immune system resist to infection and treatment of pathogens.

The researchers found that autophagy can inhibit hepatic stellate cells so that the hepatic stellate cells with active metabolism can come back to resting and quiet state. This is a new discovery of autophagy in stem cell organisms. Inactivated autophagy has a profound effect on the blood system, leading to imbalance in some types of white blood cells. Autophagy also reduces the ability of hepatic stellate cells to regenerate.

By testing in mice, the researchers found that 70% of spleen cells in aging mice did not develop autophagy and showed a dysfunction. In addition, scientists have found many different tissue stem cells, and all the performance will be reduced with age.

"This finding provides a new perspective for anti-aging, focusing on the old hepatic stellate cells and slowing down the aging blood system. And we want to find a real ability to improve stem cells themselves and use this ability to help older people and provide them with a better immune system to resist infection by preventing the development of blood diseases. Flarebio provides recombinant proteins of good quality such as recombinant Itgb5 at reasonable prices.

A new method used to treat asthma

A new study published in the Journal of Allergy and Clinical Immunology investigates a potential new approach for the treatment of asthma. According to research using recombinant human proteins, asthma causes the individual's airway to become inflamed and narrower and produce additional mucus. The patient's breathing becomes difficult, and the result is a wheezing and coughing. It is estimated that 12% of people in the United States suffer from asthma, equivalent to about 25 million people.

There is a series of potential triggers for asthma. These include pollen, mold, dust mite, animal dander, air pollution, certain medications and exercise. The current drugs can effectively treat many people's symptoms, but as the lead author of the study, Dr. Ruth Sander said, "For many people with asthma, especially severe asthma, treatment is not 100% effective. Although the study is aimed at new treatments for allergic-related asthma, it still requires new therapies for allergies that are independent of allergies, and the steady increase in asthma cases and their fatalities and the shortage of drugs in some individuals make asthma research an important area of research."

A recent study at the University of Leicester, UK, investigated the role of specific proteins in asthma, called the high mobility group box 1 (HMGB1). Researchers hope their findings may pave the way for more effective treatment. HMGB1 is a chromatin protein, meaning that it helps to tissue DNA and regulate its transcription in the nucleus. It is secreted by immune cells (including monocytes, macrophages and dendritic cells) and promotes inflammatory responses.

Current studies use mucus and muscle tissue from mild to moderate patients with asthma. It is known that the smooth muscle in the airway has a significant contribution to the symptoms of asthma; it is overly contracted and the quality is increased, and the chemicals involved in the inflammatory response are released. "As far as we know, this is the first study to show that HMGB1 has a direct effect on stimulating the increased airway muscle contraction, and this study has led us closer to improving the treatment of patients with severe asthma," Dr. Sanders continued.

This is the early stage of the study of this new approach. However, it marks an important leap; by understanding the role of HMGB1 and its role in asthma, eventually we can take new interventions. By the way, Flarebio provides you with high-quality recombinant proteins like recombinant ECEL1 at competitive prices.

Scientists have found that stimulating immune system may stop tumor growth

According to a new study, the discovery of chemicals in tumors may help to prevent tumor growth. Researchers at the University of Illinois at Chicago report that the increase in chemical cytokines called LIGHT in mice with colon cancer activates the natural killer T cells of the immune system and causes contraction of metastatic tumors in primary tumors and liver. The LIGHT is an immunostimulating chemical messenger that was previously found to have low levels of expression in patients with colon cancer metastases. The results were published in Cancer Research which has published studies on various recombinant proteins including recombinant horse proteins.

Colon cancer is the second leading cause of cancer death in the United States. "The current treatment is palliative for most patients with colon cancer who have spread to the liver," said Dr. Ajay Maker, Associate Professor of Surgery at UIC Medical School. "Although studies suggest that immunotherapy may be a form of promising way to treat advanced cancer, this treatment has not been very successful for advanced gastrointestinal metastasis."

Maker and his colleagues established colon cancer tumors in the mouse model, in which animals had a complete and unedited immune system. Once the tumor size was visible, the mice were randomized into two groups - one group turned on cytokine LIGHT in the tumor and the other group was used as a control group for comparison.

"We have demonstrated that the delivery of therapeutic immunostimulatory cytokines results in the transport of T cells into the tumor and becomes activated tumor killer cells," said Maker. "This activity is particularly exciting because it leads to a deep anti-tumor immune response having no other chemotherapy or intervention, manipulating our natural defense system to combat the tumor."

"We have not only found that LIGHT expression promotes tumor regression, and after further studies we have also identified specific types of T cells responsible for contracting tumors," said Maker, "These findings are strong and have great clinical potential." By the way, Flarebio provides you with superior recombinant proteins such as recombinant Nrg2 at competitive prices.

To use liver cells' own ability to burn liver fat

Swedish researchers are planning a clinical trial for nonalcoholic fatty liver and new therapies for type 2 diabetes - using liver cells' own ability to burn liver fat. In a study of 86 patients with varying degrees of fatty liver, researchers from the KTH Royal Institute of Technology's Life Sciences Research Center (SciLifeLab) and the University of Gothenburg found that the liver has the ability to burn and accumulate fat. The researchers suggested that a mixture could run this process. This result was published in the journal Molecular Systems Biology, which also publishes other studies on recombinant human proteins.

The researchers mapped metabolic changes in fat accumulation in 86 patients with hepatocytes and combined these data with the analysis of the liver tissue genome model to identify the precise metabolic changes experienced by different individual hepatocytes.

Adil Mardinoglu, the lead author of the study, is a systematic biologist at KTH and SciLifeLab and one of the researchers who previously linked NAFLD to low levels of antioxidant glutathione (GSH). The conceptual validation test showed that the treatment of human subjects by increasing the "cocktail" of fat oxidation and antioxidant synthesis would result in burning liver fat. "The team's metabolic modeling approach relies on data from the Swedish human protein profile that will be useful in many chronic liver disease studies," Mardinoglu said.

Based on the results of this study, improved intervention using material combination was designed. "This mixture may reduce the accumulation of fat in the liver," Mardinoglu said. "There is no such drug yet, and we plan to conduct further clinical trials later this year."

This method combines system biology with clinical medicine. "The results are exciting, and we are now designing a mixture that will promote the oxidation of fat and produce antioxidants in liver tissue," said Jan Borén, senior partner at Gothenburg University. The researchers believe that the mixture can also be used to treat alcoholic fatty liver and type 2 diabetes caused by liver fat accumulation. "Considering the common characteristics of NAFLD and diabetes usually coexisting and interacting with each other, the mixture may also be effective for people with diabetes," says Ulf Smith, a partner at Gothenburg University.

"I am delighted that the resources created through the work of human protein profiling can be used to analyze the clinical data of NAFLD and to guide the design of mixtures of clinical diseases," said Mathias Uhlén, program director for the Human Protein Atlas and co-author of the paper. Flarebio provides you with high-quality recombinant proteins like recombinant COLEC12.

A potential drug target for obesity and related metabolic diseases

Guo Fumin Research team at Chinese Academy of Sciences, Shanghai Institute of Health revealed that the new function of hypothalamic aorticoprine (POMC) neurons activating transcription factor 4 (ATF4) to regulate energy balance and lipid metabolism of the body, providing a potential drug target for obesity and related metabolic diseases. Related research results have been published online recently in the journal Diabetes. By the way, this journal is also famous for its studies involving recombinant rat proteins.

The obesity of body is caused by imbalance of energy intake and energy consumption, and it plays a key regulatory role for body energy balance in central nervous system. In the hypothalamic arcuate nucleus, there are two types of neurons that regulate energy metabolism: one is the brain-related protein neurons that promote appetite; the other is the appetite-suppressing POMC neurons. POMC neurons inhibit the appetite by releasing the melanogenesis of the melanocortin, which on the other hand affects the energy dissipation of the body by regulating the excitability of the sympathetic nervous system.

The researchers specifically knocked out the ATF4 gene in mouse POMC neurons. Analysis showed that these knockout mice became thinner, the insulin sensitivity, leptin sensitivity and energy dissipation of the body increased and they could resist obesity induced by high-fat diet, insulin resistance and leptin resistance. Further study showed that ATF4 can bind to the promoter of the ATG5 gene to directly regulate its expression. The researchers also constructed double-knock mice of the ATF4 gene and the ATG5 gene in POMC neurons. Through its phenotypic analysis, it showed that double-knock mice can reverse the phenotype of ATF4 single-knockout mice. By the way, Flarebio provides you with recombinant proteins of good quality such as recombinant ITGB2.

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.

A vaccine that would fight all mosquito-borne diseases

Ars Technica has announced an important advancement in the field of vaccines: the National Institutes of Health (NIH) announced the launch of a vaccine phase I clinical trial that would fight all mosquito-borne diseases. According to research using recombinant human proteins, the vaccine, named AGS-v, is aimed at mosquito saliva rather than individual bacteria.

Scientists have been hoping for a vaccine to fight all the mosquitoes, and the UK Sik Biotechnology Group and NIH are pushing the dream to be a reality. The Sikh Group has developed an AGS-v vaccine for decades of exploration, which allows humans to immunize all diseases spread by mosquitoes. The company believes that the vaccine is equivalent to a "weapon". If the mosquito bites the vaccination of the vaccine, it will face death or the result of not being able to reproduce. AGS-v is not usually vaccinated to prevent a particular disease vaccine but creating a "whistle" for the mosquito saliva in the human body, that is, an immune system. When the mosquito remains saliva in the human body, the immune system will produce a similar allergic reaction to "destroy" pathogens in the body.

Scientists have been thinking about targeting mosquito saliva for some time. Mosquito saliva contains a variety of proteins, and the new vaccine is developed through the four kinds of proteins that usually can be found in mosquitoes. But at present, Sikh has not yet announced related data on the safety and efficacy of the vaccine.

Mosquito is the creature which kills the most humans, far more than the sum of the numbers of other biological killers. Mosquito-borne malaria is likely to be the greatest infectious disease of great threat to human history, and it can't be eradicated so far. This strange trick came up by US and British scientists makes the human immune system attack all foreign body injected by mosquito. If it is effective and feasible, it will become another milestone in the history of human medicine, meaning comparable to antibiotics. The human immune system has great potential, making use of it to destroy all kinds of incurable diseases in the future is more hopeful than medication. By the way, Flarebio provides you with superior recombinant proteins including recombinant ECE1 at competitive prices.

Autism-related gene variations improve brain evolution

Researchers at Yale University in the United States published a paper in the journal Public Library of Genetics that the genetic variation associated with autism may be a positive choice in the evolutionary process because these variations also help to increase human cognitive ability. More research through recombinant mouse proteins should be conducted.

In the long evolutionary process, humans produce a lot of genetic variation, and the effects of these variations on human genetic characteristics are positive and negative. Those who have a negative impact on human reproduction will be eliminated in the evolutionary process; and if the emergence of mutations can improve the chance of human survival, it will become a positive choice of human beings and be retained in the genome and be passed down generation by generation.

In this study, the researchers conducted a genome-wide association study of more than 5,000 cases of autism, and they analyzed the gene selection in human evolution. They found that genetic variation associated with autism is more of a positive choice in human evolutionary processes that are not only related to autism but also to human intelligence. For example, many autistic-related gene mutations identified by the researchers can enhance brain cell function and help to create new neurons.

Researchers point out that genetic variation that increases the risk of autism is a positive choice in the evolution of humans. This may make people feel unimaginable: why do a large number of autistic pathogenic gene mutations remain in the human genome? Why don't humans eliminate them in the evolutionary process? The reason is that these variations have a positive effect on human cognitive function, so it is actively chosen in the evolutionary process, and the cost is an increase in the risk of autism. Flarebio provides you with high-quality recombinant proteins like recombinant PIGR at good prices.