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.

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.

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 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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Researchers from the Shanghai Institute of Health Sciences, Shanghai Jiaotong University School of Medicine recently used the human genome-wide transcription factor siRNA library to screen transcription factors which participate in the ESC self-renewal and found that a series of important genes which are important for maintaining human ESC, particularly the great importance and mechanism of PHB as a new member of HIRA complex in the regulation of human embryonic stem cells (embryonic stem cells, ESC) self-renewal. The study was published in the December 8 issue of Cell Stem Cell which also has other studies on recombinant human proteins, and the author of the article is Professor Jin Ying from Shanghai Jiaotong University School of Medicine.

In this study, the researchers used the human genome-wide transcription factor siRNA library to screen participants in the ESC self-renewal transcription factor and found a series of genes that play an important role in maintaining human ESC properties. They studied the PHB gene in particular. Previous studies have learned that PHB is involved in a variety of important life processes in mammalian cells. However, the function of the gene in the ESC has not been reported. The study of the Jinying group found that PHB plays an important role in maintaining human ESC self-renewal and promoting the reprogramming of human adult cells, especially PHB plays a unique role in maintaining the correct histone methylation of human ESC effect. Further studies have shown that PHBs interact with the HIRA complex of the chaperone protein H3.3 and maintain the protein stability of the HIRA complex.

In addition, the researchers found that PHB and HIRA jointly regulate the enrichment of H3.3 in the whole genome of chromatin, especially in the regulation of H3.3 in isocitrate dehydrogenases (IDHs) Gene promoter region and the expression of IDH gene to control the production of a-ketoglutarate (a-KG), a key metabolite that plays an important role in the fate of ESC, to shape the correct histones Methylation levels, maintenance of human hESC self-renewal and epigenetic characteristics.

This study reveals the key role of PHB in pluripotency regulation through genome-wide, large-scale siRNA screening, and it reported that PHB interacts with HIRA complex to regulate the enrichment of H3.3 on chromatin. This study also revealed the important regulation of HIRA complex and H3.3 on IDH gene expression and key metabolite a-KG, and proposed an apparent-metabolic regulatory loop maintained by human ESC. Flarebio provides you with good-quality recombinant proteins like recombinant ECEL1 at competitive prices.

Scientists have developed lower-cost therapy for uncommon genetic diseases

Scientists from an international research group suggested in Nature on Feb. 22 that blocking the molecules which cause Gauchers disease (GD) and other lysosomal storage disease (LSD) inflammation and organ damage can be used as a treatment, and this method is lower than the current treatment costs. More research through recombinant human proteins will be conducted.

Through the study of laboratory mouse models and human cells, the team showed that C5aR1 is a key molecular pathway in driving the inflammatory process of Goie disease. The process of inflammation of Geshe disease is initiated by the mutation of GBA1 gene. GBA1 encodes lysosomal enzyme glucocerebrosidase (GCase), which degrades the adipose molecule glucoamate (GC). C5aR1 is a small peptide (protein component) receptor from a complement system known as C5a (part of the immune system) that drives inflammation in several different types of immune cells.

Dr. Manoj Pandey, a scientist at the Syndicate Children's Human Genetics Division, and his colleagues showed that inflammatory glucose enamel accumulation in the spleen, liver, lung and bone marrow immune cells drives the self-expression of the glucose-ceramide that forms the immune complex antibody induction. These immune complexes promote the production of C5a and the activation of its receptor C5aR1.

Based on the evidence that C5aR1 participates in the process of Goie's disease, the researchers decided to test targeted molecular pharmacology in laboratory mouse models. Using C5aR antagonists (C5aRA) developed by K?hl, scientists injected C5aRA into the peritoneal cavity of mice. In the lung, liver and spleen of mice, the infiltration of proinflammatory immune cells (macrophages) is substantially reduced, and the accumulation of glucose-ceramide is almost completely eliminated.

Because the current project was carried out in mouse models and human blood cells, Pandey and his colleagues stressed the need for additional research before determining whether C5aR1 is effective and safe enough to be tested in human patients.

Pandey said the researchers will continue to test the C5aRA molecules used in mouse studies that are effective in targeting human and mouse C5aR. They will also test commercially available anti-C5 monoclonal antibodies called eculizumab and produced by Alexion Pharmaceuticals, which helped finance this study. This will allow researchers to test these compounds as a neoadjuvant therapy for human patients with Gaucher and other lysosomal storage diseases. Flarebio provides you with high-quality recombinant proteins such as recombinant Nrg2 at competitive prices.

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.

A convincing scientific evidence for the Zika virus leading to microcephaly

In recent years, Brazil and other countries in the Americas frequently show microcephaly. According to studies on recombinant human proteins, the scientific community has confirmed that the Zika virus infection shows some association with the incidence of microcephaly, but they don't know how the virus impacts fetal brain development. German researchers have said that they have found the scientific evidence of Zika virus that causes microcephaly.

Researchers at the University of Cologne, Germany, and other institutions reported in a new issue of Cell-Stem Cells that they "reprogrammed" healthy human skin cells into cultured pluripotent stem cells to culture neural precursor cells. Neural precursor cells can differentiate a variety of nerve cells and can be described as the "starting point" of brain development.

Under specific experimental conditions, the researchers gathered many neural precursor cells into brain organs, that is, a few millimeters in size with three-dimensional structure of the brain tissue fragments. The process of embryonic brain simulates the early development and observes the virus effect of infection on embryonic brain development.

The results showed that Zika virus allows cells to involve in cell division - the central body shows failure so that nerve precursor cells prematurely differentiate into mature nerve cells. This "precocious" seems to be of no harm, but it will make a lot of nerve precursor cells no longer involve in brain organ growth into a complete brain process, leading to microcephaly.

Researchers said that they used Zika virus strains isolated from the small head deformed embryos in the experiment, and the experimental results provide a convincing scientific evidence for the Zika virus leading to microcephaly.

Zika virus spreads mainly through Aedes aegypti, but it is also sexually transmitted. People infected with Zika virus may show fever, rash, joint pain and other symptoms similar to dengue fever. The vast majority of infected patients are mild, but pregnant women need to be careful. Once infected, it may lead to fetal malformations. Flarebio provides you with good-quality recombinant proteins including recombinant TLR2 at competitive prices.

Adipocytes play an important role in human body

Adipocytes are not simply large in the presence of large amounts of lipids in the body, whereas they emit hormones and other signaling proteins that affect many other types of tissues. In a new study in the United States, scientists have determined through research using recombinant human proteins that adipocytes can deliver microRNAs through the exosomes pathway and regulate other organs. This suggests that fat cells are promising in the use of gene therapy for metabolic diseases such as fatty liver disease.

Professor Ronald Kahn from the Joslin Diabetes Center published a study on Nature on Feb. 15 that revealed that the mechanism which could provide a potential for new treatments to develop the possibility of using adipocytes to develop gene therapy to help treating the liver or other organ metabolic diseases, cancer and so on.

MicroRNAs are not translated into proteins but can regulate other RNA to produce proteins. All cells of our body can produce microRNAs, and some of these microRNAs are known to be released from the cells into the bloodstream. However, once they enter the blood, what they have done is what scientists have been arguing about.

Joslin scientists have focused on microRNAs from adipocytes that are released into the blood through the "exosomes" pathway. Researchers have constructed a genetically modified mouse model that prevents adipocytes from producing microRNAs. Joslin researchers later found that the number of circulating microRNAs in the exosomes decreased significantly in mice that did not originate from adipocyte microRNAs. This reduction in the number of circulating microRNAs can be restored when the investigator transplanted normal fat into these mice, indicating that most of the circulating microRNAs were from fat.

Next, the scientists studied two forms of fat malnutrition: fat loss or hereditary fat metabolism. In both groups, they found that circulating microRNA levels in exosomes were below normal levels. "This suggests that these circulating microRNAs produced by fat may help diagnose metabolic diseases such as obesity, type 2 diabetes and fatty liver disease," Kahn said. Flarebio provides you with good-quality recombinant proteins including recombinant COLEC12 at reasonable prices.