Zinplava drug of Merck has been approved by FDA

The FDA clarified the efficacy of Merck's Clostridium difficile (CDI) relapse drug Zinplava after a three-month extension of the review period. Merck said it expects Zinplava to be available in the first quarter of next year.

Through research using recombinant human proteins, patients with Zinplava (17.4% and 15.7%) or Zinplava and actoxumab (15.9% and 14.9%) had a significantly lower recurrence rate at week 12 than patients taking placebo (27.6%) in a phase III study of Pivotal (25.7%). Thus, Zinplava (bezlotoxumab) is thought to reduce the recurrence of CDI in patients aged 18 years or older who have received antimicrobial therapy and have a high risk of recurrence.

The company emphasizes that its drug is not an antibacterial agent, and therefore it can't be used in the actual treatment of infection. But rather a monoclonal antibody for neutralizing Clostridium difficile toxin B, which may damage the intestinal wall and cause inflammation, leading to diarrhea.

At the same time, about a quarter of patients have a recurrence after the first episode, and more than 40% of patients have a recurrence, indicating a need to continue looking for new ways to break the cycle of infection.

According to the US Centers for Disease Control and Prevention, the data show that only in the year of 2011, Clostridium difficile caused nearly 500,000 cases of infection in the United States, of which 29,000 people died within 30 days after the initial diagnosis. Flarebio offers recombinant proteins of good quality like recombinant Cdh9 at competitive prices.

Researchers successfully conduct mice experiment to cure autism

A team composed of Prof. Fukuda Mishi and Prof. Liu Mao from the Department of Life Science, Tokyo Pharmaceutical University successfully discovered through recombinant rat proteins that a new-type protein CAMDI in a study which can bind to DISC1. It was confirmed by other research teams that the CAMD1 gene is likely to be the genetic risk genes which lead to serious mental illness. CAMD1 mutation and psychiatric disorders are associated with abnormal behavior.

Researchers produced CAMDI gene-defected mice in advance and analyzed them. They found that the cortical neuron cells of this mouse showed slow movement, and this phenomenon is also one of the main causes of developmental disorders. Behavioral observation of mice showed that they were hyperactive, repetitive movements and unable to adapt to the new environment and lacked for social and other typical autistic behavior. In addition, the researchers also found that CAMD1 can control enzyme activity of deacetylase inhibitor HDAC6. CAMDI gene defect can cause HDAC6 abnormal activity, which directly results of regulation of nerve cell migration center immature, and nerve cell migration becomes slow.

In further study, the team members conducted HDAC6 inhibitor administration to the fetal brain cells cerebral cortex at the motor phase. Follow-up observation can be found in these mice that nerve cell recovery returned to normal, and hyperactivity, repetition, and the ability to adapt to new environments and other issues have been restored.

In the HDAC6 enzyme activity inhibitor, there is a skin T cell lymphoma treatment drug called "SAHA (alias: Vorinostat)" has been widely recognized in drug repositioning (Drug repositioning) and is expected to be used as a therapeutic agent for mental disorders. The researchers said they will explore the SAHA application trials and strive to develop new therapies. The details of this study have been published in EMBO, the official journal of the European Molecular Biology Organization. Flarebio provides good-quality recombinant proteins such as recombinant Cdh9 at great prices.

The way of cells converting food into energy

It is known to all that the way in which cells convert food into energy is so common among all living things. It puzzled scientists for a long time. Now scientists have discovered a likely reason why the way is shared so widely.

Researchers conducted research through recombinant proteins such as recombinant rat proteins and digested simple sugars such as glucose in a series of chemical reaction to examine how cells make energy from food. The process is almost the same for every kind of cell, including animals, plants and bacteria.

Their news study shows that this process is the most effective way to extract energy. Cells that have more energy can grow and renew faster, giving them and the organism to which they belong an evolutionary advantage.

Scientists at the University of Edinburgh built some complex models to better understand why cells develop the pathways they use to convert sugar into energy. They compared the models in animals and plants with alternative mechanisms that might have evolved instead. They conducted a detailed search for all possible alternatives to the established biological mechanisms known to have existed for billions of years. The results show that the metabolic systems have evolved because they enable cells to produce more energy, compared with alternative pathways.

The key mechanisms that underpin metabolism are found in almost all plants and animals and control the productivity of life on Earth. Although we understand little of how the mechanisms came about, this study shows that our metabolic pathway is a highly developed solution to the problem of how to extract energy from our food, According to Dr. Bartomiej Waclaw from the University of Edinburgh's School of Physics and Astronomy who took part in the study published in Nature Communications. Flarebio provides recombinant proteins of good quality such as recombinant Cdh9 at great prices.

A new diagnostic method has been developed

Parkinson's disease is a common neurodegenerative disease. There are more than two million patients in China, and the incidence in the elderly over 65 years is about 1.7%. Parkinson's disease mainly affects human motor function, and its common symptoms include slow movement, limb rigidity, tremor at rest posture and gait disorders. Many patients also have sleep disorders and anxiety symptoms. Parkinson's disease. For the problem of early diagnosis, British scientists recently released a method of early diagnosis of Parkinson's disease by detecting cerebrospinal fluid.

This method developed by researchers from the University of Edinburgh makes use of a lot of recombinant proteins such as recombinant mouse proteins and is aimed at one of the culprits for Parkinson's disease - a protein called α-synuclein. α-synuclein protein can be combined with each other in the nerve cells to form a structure called Lewy body. Lewy body would damage the normal function of nerve cells, leading to Parkinson's disease and Lewy body dementia which is closely related to Parkinson's disease. The difficulty of detecting α-synuclein lies in that normal nerve cells also produce this kind of protein. Only when its viscosity shows changes, they would combine with each other to form Lewy bodies.

Researchers at Edinburgh University used a technology called real-time vibration-induced conversion (RT-QuIC) to specially detect those α-synuclein proteins which are more easily to bind to each other with higher viscosity. In early experiments, this detection method successfully diagnosed 19 cases from 20 cerebrospinal fluid samples of patients with Parkinson, and the accuracy rate of 95%. While in 15 control samples, none showed false positive, and the specificity was 100%. What's more important, this test successfully separated the Lewy body dementia and Alzheimer's disease in the control group samples, showing its sensitivity and specificity.

The corresponding author of the study, Dr. Alison Green at University of Edinburgh said, "We have successfully applied this technology which had been proved in the diagnosis of BSE to Parkinson's disease. We hope to further improve it to help it better apply to the early diagnosis of Parkinson's disease. The earlier the diagnosis is, the earlier the treatment can help patients sooner to participate in the latest clinical trials."

Next, the researchers plan to start a large-scale clinical diagnostic test for Parkinson's disease in order to achieve the same high accuracy and specificity. We hope that this method of early diagnosis can be put into practice as soon as possible to help patients to start treatment as early as possible in order to obtain better results. Flarebio provides you with high-quality recombinant proteins like recombinant Cdh9.

The mechanism of YTHDF2 accelerating polyadenylation and degradation of RNA

YTHDF2 binds to m6A modification on RNA and recruit CCR4-NOT adenylate cyclase complex through direct interaction with CNOT1 to accelerate polyadenylation and degradation of RNA, according research using recombinant mouse proteins.

On August 25th, the international academic journal Nature Communications online published the latest study collaborate by Wu Ligang study group from the Shanghai Life Science Institute of Biochemistry and Cell Biology Institute of the National Academy of Sciences Protein Science Center (Shanghai) and Life Sciences and Ma Jinbiao study group from School of life sciences of Fudan University - YTHDF2 destabilizes m6A-containing RNA through direct recruitment of the CCR4–NOT deadenylase complex. The study found that YTHDF2 promotes RNA containing m6A to degrade by directly recruiting CCR4-NOT complex adenylate cyclase complex.

Methylation located at the site of adenylate N6 (m6A) is the most common type of modification inside of eukaryotic mRNA and the long non-coding RNA. Recent studies show that m6A is a dynamically-reversible RNA modification which plays an important role in many biological processes, including stem cell self-renewal and differentiation, reproductive mice, yeast meiosis and the like. m6A can be identified by a variety of intracellular proteins and can binds to them, thereby regulating the processing, translation and stability of RNA. Wherein m6A binding to protein YTHDF family can contribute to the degradation of RNA, but the RNA degradation pathway and molecular mechanism mediated by it are still unknown. The research made use of momentary inducible expression system to monitor the degradation process of RNA, and it was found that m6A modification or YTHDF2 binding all can promote the RNA deadenylation (i.e., the removal of RNA 3 'end poly (A) tail).

Researchers conducted interaction detection and functional screening on a variety of adenylate cyclase in cells of mammalian and ultimately determined the CCR4-NOT adenylate cyclase complex is the effector which mediates the process. CCR4-NOT is a nine-subunit complex comprising adenylate cyclase CAF1 and CCR4 which have catalytic activity and scaffold protein CNOT1. Further studies have shown YTHDF2 directly interacts with SH domain of CNOT1 through its N-terminal region to recruit CCR4-NOT complex. As the main adenylate cyclase, CAF1 and CCR4 promote the polyadenylation and degradation of m6A RNA.

Interestingly, not only m6A modification located in mRNA 3' non-translated region can lead to degradation of mRNA, m6A modification located at protein reading frame (ORF) of mRNA, and m6A modification in long non-coding RNA in are also leads to its RNA degradation by the same mechanism. The study reveals the molecular mechanism of m6A modification- mediated degradation of mRNA and lncRNA, doing more help for clarifying the phenomenon of RNA modification regulating gene expression. Flarebio provides good-quality recombinant proteins like recombinant Cdh9 at competitive prices.

The mechanism of gene defect causing to autism in mice experiments

A Japanese research team found the pathogenesis of gene defect leading to autism in mice experiments, which will help to treat autism.

Kyushu University in Japan issued a statement on 8th after a series of studies using recombinant mouse proteins, saying that autism is a common type of developmental disorder mental illness, and its specific pathogenesis has been unclear. Previous studies suggest that it may be caused by fetal neurodevelopmental disorders. In recent years, genetic studies of autism show that chromatin remodeling factor CHD8 is a gene which has the highest rate of mutation. A research team of this school made CHD8 genes of lab mice show the same mutation like human patients and found that mice also showed symptoms similar to the symptoms of human autism such as abnormal exchange, stubbornness, etc.

The study found that CHD8 mutation made a protein called REST in the mice very active. This protein is very important for neural development, and its abnormal activity may lead to hyperactive neurodevelopmental delay.

The team believes that this discovery shows that it may be possible to treat autism by inhibiting protein REST or related methods. The research results have been published in the British journal Nature. Flarebio provides you with recombinant proteins of good quality such as recombinant Cdh9 at good prices.

A small molecule that can help to reduce AML relapse

Researchers have made a small molecule that could deliver a one-two punch to proteins that resist chemotherapy in patients with AML. The researchers are from Rice University, Baylor College of Medicine and the University of Texas MD Anderson Cancer Center. It may be the key to helping patients who are fighting acute myeloid leukemia (AML) avoid a relapse. There are many kinds of recombinant proteins such as recombinant horse proteins used in the research.

The work led by Rice chemist Zachary Ball, Baylor pediatrician Michele Redell and MD Anderson oncologist David Tweardy appears this week in the journal Angewandte Chemie.

The protein STAT3, interferes with chemotherapy by halting the death of cancerous cells and allowing them to proliferate. The molecule locates and attacks a previously unknown binding site on STAT3, thus disrupting its disease-promoting effects.

The STAT3 protein stands for "signal transducer and activator of transcription 3". It is a suspected factor in the relapse of nearly 40 percent of children with AML. The new proximity-driven rhodium(II) catalyst known as MM-206 finds and modifies an inhibitor-binding site on the protein's coiled coil -- literally protein coils coiled around each other -- and delivers the inhibitor, naphthalene sulfonamide, to the modified site.

"We know that increased activity of STAT3 in AML and other cancers helps the cancer cells survive chemotherapy, so any new strategy we can develop to stop that process could mean real benefit for our patients," said Redell, who is also part of the leukemia and lymphoma teams at Texas Children's Hospital.

"Our main advance, from a medicinal perspective, is that this compound also works in a mouse model," Ball said. "All the other compounds worked in cells, but in mice, they weren't potent enough or stable enough."

Follow-up studies should lead to improved versions of the complex. The new discovery is of great importance showing the way to future anti-cancer approaches. Flarebio provides you with good-quality recombinant proteins such as recombinant Cdh9 at good prices.

Protein makes sense in a cell

More than a decade ago scientists found the sequencing of the human genome, and it was undoubtedly considered one of the greatest discoveries in biology. However, it was only the beginning of our in-depth understanding of how cells work. Genes are just blueprints and it is the proteins, genes' products that do much of the work in a cell. With the use of recombinant proteins like recombinant mouse proteins and recombinant horse proteins, a multinational team of scientists have sifted through cells of vastly different organisms, from amoebae to worms to mice to humans, to reveal how proteins fit together to build different cells and bodies.

The wonderful finding is a result of a collaboration between seven research groups from three countries, led by Professor Andrew Emili from the University of Toronto's Donnelly Centre and Professor Edward Marcotte from the University of Texas at Austin. The study uncovered tens of thousands of new protein interactions, accounting for about a quarter of all estimated protein contacts in a cell.

If one of these interactions is lost it can lead to disease, and the map can help scientists spot individual proteins that could be at the root of complex human disorders. Through open access databases, the data will be available to researchers across the world.

Proteins work in teams by sticking to each other to carry out their jobs. Many proteins come together to form so called molecular machines that play key roles, such a building new proteins or recycling those no longer needed by literally grinding them into reusable parts. But when it comes to the vast majority of proteins, for example, there are tens of thousands of them in human cells, we still don't know what they do. There are a lot of researchers interested in recombinant proteins focused on this topic.

Then Emili and Marcotte's map helps. Using a state-of-the-art method developed by the groups, the researchers were able to fish thousands of protein machineries out of cells and count individual proteins they are made of. They then built a network that, similar to social networks, offers clues into protein function based on which other proteins they hang out with. For example, a new and unstudied protein, whose role we don't yet know, is likely to be involved in fixing damage in a cell if it sticks to cell's known "handymen" proteins.

The study gathered information on protein machineries from nine species that represent the tree of life: baker's yeast, sea anemones, amoeba, flies, sea urchins, worms, frogs, mice and humans. The map expands the number of known proteins association over tenfold, and it will trace how they evolved as time goes on.

The researchers discovered that tens of thousands of protein associations remained unchanged since the first ancestral cell appeared, one billion years ago (!), preceding all of animal life on Earth. The researchers believe that, with tens of thousands of other new protein interactions, the map promises to open many more lines of research into links between proteins and disease, which they are keen to explore in depth over the coming years.

The study comes out in Nature on September 7. Protein assemblies in humans were often identical to those in other species, thus the study will provide the ability to study the genetic basis for a wide variety of diseases and how they present in different species. Hope more secrets can be found. Flarebio offer good-quality recombinant proteins of good quality such as recombinant Cdh9 at good prices.

Researchers find two Zika virus proteins related to microcephaly

Researchers from the University of Southern California said on 11th this month that they have found two Zika virus proteins related to microcephaly, stepping one small step further towards preventing pregnant women with infection of Zika virus from giving birth to babies with microcephaly. They conducted related research using recombinant rat proteins and recombinant horse proteins.

The study is published in the new issue of the US journal Cell Stem Cell. As one of study leaders and assistant professor at the University of Southern California, Zhao Zhen said that the goal of this study is to find the molecular mechanism of Zika virus inhibiting brain development that is to analyze which Zika virus protein can kill or inhibit the neural stem cells. Zika virus is relatively small virus which only contains 10 proteins. They found that NS4A and NS4B proteins may be associated with microcephaly.

Zhao Zhen said that the two proteins are capable of regulating so-called Akt-mTOR signal pathway within the cells and inhibit human embryonic neural stem cell proliferation and differentiation, and they can also improve autophagy function of cells to accelerate replication of Zika virus, which may lead to microcephaly. "This is only the first step we have taken," he said, "According to the available data, we can only conservatively say that these two proteins are likely to be associated with microcephaly. To prove how they result in microcephaly, there are many experiments to do."

As for the significance of this discovery, he said that this is the first report of discovering Zika virus protein related to microcephaly, providing a target goal for future head disease prevention and treatment research. But there is still a long way to go to the clinical application. He noted that in the view of prevention, Zika vaccine may be the most viable option. As for whether these two proteins are also associated with other birth defects, it is still unclear. Flarebio provides you with good-quality recombinant proteins including recombinant Cdh9.

Knocking out a target can improve effect of cancer drugs

Recently scientists find in the process of studying skin cancer, leukemia and other types of tumors that some anti-cancer drugs which block the Hedgehog signaling pathway also have great potential in terms of blocking tumor proliferation, and many anticancer drugs take this signaling pathway as a target. But according to some research using recombinant mouse proteins, some with the clinical use of drugs, people gradually found that some tumors become resistant to this.

A * STAR cellular and molecular biology researchers have discovered a new target - once the target was knocked out, it will remove the resistance of cells to Hedgehog signaling pathway drug and improve the therapeutic effect. The main director of the project Philip Ingham said, "Inhibiting the activity of the target protein can block the Hedgehog activity in cells. Then we can greatly reduce drug resistance of tumors by the combination therapy of several drugs."

Hedgehog signaling pathway plays an important role in the growth and differentiation of embryonic cells, but the elevation of its activity in adult tissue can easily cause cells to become cancerous. Currently, vismodegib and sonidegib are important cancer drugs aiming at Smoothened protein in the Hedgehog signaling pathway and are mainly used in skin cancer. To avoid resistance of these drugs, the drugs in the downstream of Smoothened protein are also under research and development. Ingham and his colleagues focus on the GRK2 protein. Through experiments on zebrafish model, they have fully understood the functions of in this protein.

In early stage of experiments, scientists silenced the gene and found a lot of changes in the Hedgehog signaling pathway. Ingham said, "Our study emphasizes the importance of the mutant allele, GRK2 protein phosphorylation by way of regulation of Hedgehog signaling activity path. But with further research, we feel GRK2 protein can link with other proteins and regulate backwards signaling pathway."

Research indicates that since the GRK2 protein won't directly interact with Hedgehog, there may be some side effects in the end. Flarebio provides high-quality recombinant proteins such as recombinant Cdh9 at competitive prices.

The study of female germline stem cells has achieved new progress

Researchers from School of Biomedical Engineering of Shanghai Jiaotong University and Bio-X Institute conducted the research of epigenetic spectrum of female mouse reproductive stem cells and found the epigenetic regulation mechanism which decides basic biological characteristics of the cells. Related study was recently published online in the journal Genome Biology, which also published a lot of studies about recombinant proteins such as recombinant mouse proteins.

Conventional wisdom holds that the produce of oocytes of vast majority of female mammals occurs only in the fetal period, and the number of oocytes doesn't increase after birth but decreases by years, which means that there are no germline stem cells in ovarian after birth. Do female mammals have germ stem cells? If so, what is the molecular mechanism that decides stem cell characteristics of development unipotency and undifferentiation?

Zhao Xiaodong study group from Shanghai Jiaotong University and Wu Ji study group from Bio-X Institutes Jiaotong University conducted collaboration and discovered female reproductive stem cell-specific histone modifications label of mark enhancer; more importantly, this study reveals DNA methylation determines developmental unipotent of female reproductive cells as a major epigenetic regulatory mechanism by inhibiting the development process of somatic cells. And it also involves in the maintenance of their female gender identity. At the same time, the researchers also found that germ cell-related factor PRMT5 also plays an important role in maintaining undifferentiated state of female reproductive stem cells. Flarebio also provides recombinant proteins such as recombinant Cdh9 at good prices.

Scientists find a new compound which can kill drug-resistant cancer cells

Many cancer deaths are because that cancer has resistance to chemotherapy drugs, which also contributed to the development of overcoming this obstacle in the field. Although more and more recombinant human proteins are developed to fight against cancer, it is no enough. A latest research shows that researchers have discovered a new compound that can kill multidrug resistant cancer cells in mice. The team includes members from Pamplona of Navarre, Spain and Krakow, Poland Jagiellonian University School of Medicine, and they published their findings in the journal Bioorganic and Medicinal Chemistry.

Lead author from the University of Navarra and the Jagiellonian University Dr. Enrique Dominguez said, "Our study reports a new method of fighting against cancer with drug resistance. We know there is more research to be conducted, but we are pleased to be able to develop new possibilities and we feel delighted on these results."

The new study came from 57 kinds of compounds which were identified as having anti-cancer properties, the team believed some of which may enhance the effectiveness of chemotherapy drugs. The study focuses on the so-called "efflux pump", which is exposure to cancer chemotherapy to develop a common defense mechanism. Located within the cell membrane, efflux pump is a protein which excludes toxic compound out of cells, and such a protein is called ABCB1. In the study, recombinant mouse proteins and recombinant rat proteins are widely used.

The team wanted to see whether selenocompounds which was found in previous studies can block ABCB1 efflux pump. After multidrug resistance (MDR) in murine T cell lymphoma running a variety of in-vitro experiments, the researchers found that these compounds can prevent efflux pump more effectively than other compounds. They also found that these compounds can trigger cancer cell apoptosis and cell suicide. The most active selenocompounds cab kills about 80 percent of cancer cells in mice.

They acknowledged that the results are only the beginning of the long process of developing a new drug, and the next step will be to conduct vivo experiments on these compounds. Flarebio offers high-quality recombinant proteins such as recombinant Cdh9. Welcome to get more information on its official website.