The genetic changes of the most common cancer subtypes B-ALL

The International Study Group from St. Jude Children's Research Hospital, the University of Washington Pediatric Cancer Genome Project (PCGP) and the Children's Oncology Group (COG) identified the genetic changes of the most common cancer subtypes B-precursor acute lymphoblastic leukemia (B-ALL) through recombinant dog proteins. In this disease, two transcription factors, DUX4 and ERG, are genetically altered, and these proteins closely control the activity of other key genes in human blood cells. The results of the study were published in the October 24 issue of Nature Genetics.

Scientists have discovered a unique mechanism that can explain how transcription factors contribute to the development of leukemia. "Our work reveals that there are a series of molecular events in B-ALL that involve the interaction of two transcription factors," said Charles Mullighan, author of the article, and author of St Jude's Pathology.

Transcription factor is a protein that binds to a particular DNA sequence and regulates the expression of genetic information from DNA to mRNA. ChIP sequencing, a method that allows researchers to analyze how proteins interact with DNA, and it is the key to revealing the relationship between two transcription factors. Sequencing studies revealed that the rearrangement of the transcription factor gene, DUX4, occurred in all B-ALL cases, resulting in high levels of DUX4 expression. DUX4 binds to the gene of the transcription factor ERG, resulting in downregulation of ERG expression. Downregulation of ERG expression impairs ERG function by deletion of part of the gene or by expression of another form of ERG (ERGalt). In both cases, loss of ERG transcription factor activity was observed, which resulted in leukemia.

"The discovery of the relationship between DUX4 fusion and aberrant ERG isoforms uses a novel computational approach developed by us that combines whole-genome sequencing, RNA-seq and ChIP," said Jinghui Zhang, PhD, Department of Computational Biology, St. Jude's first author. "The genomic landscape of B-ALL subtypes can also be visualized using ProteinPaint (pecan.stjude.org), a powerful interactive tool developed by St. Jude and it is used to examine pediatric Cancer mutations and gene expression.

"Our data show that DUX4 gene rearrangement is present in all patients with different gene expression profiles," said Li Ding, co-author of the paper and assistant director of the McDonnell Genome Research Institute and director of computational biology at the University Of Washington School Of Medicine in St. Louis. The gene rearrangements are cloned in the early stages of leukemia.

Stephen Hunger, co-author of the paper said that genetic defects in this relatively common B-ALL subtype were not fully understood until DUX4 abnormalities were found. "These results underscore the need for more knowledge of genetic variation in ALL, which can help to improve patient care," he said.

The researchers hope that the determination of the relationship between the two transcription factors will lead to the emergence of new diagnostic tests. Even with other deleterious genetic mutations, DUX4 / ERG ALL were associated with a favorable outcome. Currently, only transcriptome or genome sequencing helps to identify DUX4 rearrangements. "Other detection methods, such as fluorescent hybridization or microscopic examination of chromosomes (karyotype analysis), are not sufficient to identify genetic changes in DUX4", scientists said. Flarebio offers recombinant proteins such as recombinant Cdh10 at competitive prices.

To combine artificial intelligence with the development of anti-cancer drugs

According to the review of Massachusetts Institute of Technology Technology, the US Department of Defense has announced that it will work with the bio-pharmaceutical company Borg Health to make use of artificial intelligence technology to carry out new drug research to find treatment programs of invasive breast cancer which existing drugs can't respond to. The research process will involve recombinant proteins such as recombinant human proteins.

The partnership will support the White House Cancer Luna program, which will screen up to 250,000 samples for new biomarkers and biomarkers for early cancer. According to the National Cancer Institute, breast cancer mortality has declined steadily over the past 20 years, but it remains the second killer of cancers of American women.

Under the terms of the agreement, Borg will have access to the US Department of Defense's clinical breast care program library, which houses 13,600 samples of nearly 8,000 healthy and diseased patients.

Borg's researchers will use a centrifuge to process the laboratory samples. Borg has developed an artificial intelligence platform to rapidly screen patient tissue samples for potential drug targets. The researchers first genetically sequenced samples from healthy donors and samples from a variety of breast cancer subtypes to establish genomic information about mutations, proteins and cellular processes present in cancer cells and normal cells. These data will be combined with the patient's known medical history into the artificial intelligence platform to establish different models of healthy and diseased tissue using tens of thousands of data points. The platform's algorithm will eventually find hotspots in the molecular signatures across these models. These hotspots may represent biomarkers or drug targets.

Niven, co-founder, president and chief executive officer of Borg said, "On contrary to conventional drug development process, the new project will start from the data and generate hypothetical drugs through the data. Narayin believes that there are still some subtypes of breast cancer that have not been identified, the new project may help to identify these unknown subtypes and known subtypes of drug targets. The key biomarkers found in the new project can help identify breast cancer by blood tests, which are less invasive than current biopsy procedures. Flarebio offers recombinant proteins of good quality such as recombinant Aplp2 at competitive prices.

Nature: MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models

Medical research scientists have been trying to find a new type of "generic" drugs or methods that can effectively kill tumor cells and can be used for the treatment of acute myeloid leukemia, lymphoma and multiple myeloma and other blood type cancer and can also be used in melanoma, Lung cancer and breast cancer. Achieving this ideal seems to be gaining momentum. A related international collaborative study appears in the recent top journal, Nature, and it is entitled "The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models". The journal also publishes other studies on recombinant rat proteins.

This "miracle" compound is called S63845 and it targets the BCL2 family of proteins, MCL1 (pro-survival bone marrow cell leukemia 1), which is essential for cancer cell survival.

Professor Guillaume Lessene from the Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, Professor Andrew Wei, a hematologist from Melbourne Alfred Hospital and Dr. Donia Moujalled from the Servier Research Institute of Medicinal Chemistry, Hungary, led their team to collaborate on the study, The results showed that S63845 is not only effective for several types of cancer, but also has good tolerance for normal cells.

Tumor cells develop and sustain their growth by avoiding programmed cell death. MCL1 is overexpressed in many cancers, but targeting the small molecules of the proteins has been challenging in clinical trials. The small molecule described in this study, S63845, can bind to the BH3 binding domain of the MCL1 protein with high affinity and specificity. Mechanistically, the scientists have shown that S63845 effectively kills MCL1-dependent cancer cells, including multiple myeloma, leukemia, and lymphoma cells by activating the BAX / BAK-dependent mitochondrial pathway. In vivo, S63845 exhibits potent antitumor activity with an acceptable safety factor as a single agent for a variety of cancers. In addition, through alone or in combination with other anti-cancer drugs, the researchers found that inhibition of MCL1 function can also be effective for several solid cancer-derived cell lines.

Professor Guillaume Lessene believes that this work provides the first clear preclinical evidence that inhibition of MCL1 is effective against a wide range of cancer types. "MCL1 is important for many cancers because it is a pro-survival protein that allows cancer cells to escape programmed cell death - a process that normally acts to remove cancer cells from the body, which is currently being carried out in a variety of cancer models. Extensive studies have shown that S63845 effectively targets survival of MCL1-dependent cancer cells, "Professor Lessene said.

Olivier Geneste, Ph.D., director of oncology at Servier, said that MCL1 was considered a valuable yet highly challenging target for preclinical studies and could be used to design drugs for this target important basis. "S63845 was discovered in collaboration with Vernalis and based on the discovery technology of fragments and structures," he said. "Servier and Novartis are collaborating on such targets. As part of the project, the clinical development of MCL1 inhibitors is expected to be launched in the near future. Flarebio provides you with good-quality recombinant proteins such as recombinant ITGB2 at good prices.

A hookworm-secreted protein has potential therapeutic value for human allergy

Recently, the Australian Institute of Tropical Medicine and Health scientists find the protein AIP-2 which can strongly inhibit immune response from the hookworm-secreted proteins through recombinant human proteins. The respiratory cell studies of animal asthma models and human allergic patients both proved that the protein has a strong anti-inflammatory effect. AIP-2 can reduce the dendritic cells co-stimulator expression and can inhibit human T cell proliferation. It was found that this protein secreted by human parasitic hookworm may be a powerful anti-inflammatory molecule, which may bring new strategies for the treatment of autoimmune diseases such as allergies. The study was recently published in the journal Science Translational Medicine.

Now, scientists' understanding about hookworms has evolved from enemies into human-disease-fighting allies, and these parasites may have molecules that cure disease. Sporadic studies of Crohn's disease and celiac disease, as well as some patient-selected parasite treatments, suggest that these parasites have molecules that can alleviate autoimmune diseases. Immunologist Severine Navarro from James Cook University at Australia are looking for disease treatment molecules in the insects. Her research which suggests that anti-inflammatory protein AIP-2 is one of them. AIP-2 inhibits airway inflammation in a murine model of asthma. This molecule also inhibits the proliferation of lymphocytes in the blood of human allergic patients.

The key to this study was the work of the molecular parasitologist AlexLoukas, which demonstrated that the molecule was not a component of the worm itself, but rather a molecule secreted by these hookworms. The researchers will hook worms in the culture dish, and then freeze the worms and these worms to swim the liquid, worm worms crushed and culture fluid were injected to asthma animals. It was found that these cultures were more effective than the parasites themselves, suggesting that anti-inflammatory molecules are mainly the secretion of these insects or excretion of components. One of Navarro's students demonstrated this phenomenon with an animal model of colitis. They used asthma mice to verify this effect. It was found that the effect of this culture medium on asthmatic asthma was astonishing. The latest study conducted proteomics analysis on the composition of this culture medium and found about 100 kinds of proteins from the liquid, of which AIP-2 is the most abundant ingredients. Navarro et al. continued the analysis of this molecule. Since the amount of this protein from the culture medium is very limited, they analyzed the protein sequence and then used molecular biology techniques to make more such molecules. Using this molecule to treat asthma mice, the results found that this molecule can have a significant effect on lung function and immune function. Navarro himself said that almost all animals can be cured of asthma.

They also found that AIP-2 mainly play an anti-inflammatory effect through the regulation of different immune cell balance, such as T lymphocytes and dendritic cells. AIP-2 can also inhibit the proliferation of T lymphocytes in human allergic patients, indicating that this molecule has potential therapeutic value for human allergy. Flarebio offers recombinant proteins of good quality such as recombinant CDH2 at great prices.

How does a plant synthesize cellulose?

Scientists now are able to watch the interior cells of a plant synthesize cellulose for the first time by tempting the cells to grow on the plant's surface using recombinant proteins like recombinant horse proteins.

"The bulk of the world's cellulose is produced within the thickened secondary cell walls of tissues hidden inside the plant body," says University of British Columbia Botany PhD candidate Yoichiro Watanabe, "So we've never been able to image the cells in high resolution as they produce this all-important biological material inside living plants."

Cellulose is the most abundant biopolymer on earth. It is the structural component of cell walls that enables plants to stay upright. Cellulose is a very important resource for producing pulp, paper, textiles, building materials, and renewable biofuels.

According to UBC botanist Lacey Samuels, one of the senior authors on the paper, plants have to lay down their secondary cell walls very quickly once the plant has stopped growing to be structurally sound. The study shows that plant cells need both a high density of the enzymes that create cellulose, and their rapid movement across the cell surface make all the process happen very fast.

"This is a major step forward in our understanding of how plants synthesize their walls, specifically cellulose," says Mansfield. "It could have significant implications for the way plants are bred or selected for improved or altered cellulose ultrastructural traits - which could impact industries ranging from cellulose nanocrystals to toiletries to structural building products."

The lead author of the paper is Yoichiro Watanabe mentioned above. The paper is published this week in Science. Flarebio offers recombinant proteins of good quality like recombinant Pigr.

Scientists find new therapeutic target of Obesity and type 2 diabetes

Obesity and type 2 diabetes are two interrelated kinds of metabolic diseases which do serious harm to the health of contemporary population, and it can lead to coronary heart disease, stroke, fatty liver, neurodegenerative and other complications. If we can try to balance the energy consumption-intake trend more toward the consumption of this end of the tilt, then it will be able to significantly alleviate the symptoms of the disease. White adipose tissue is the main place to store fat in the human body. It can produce "browning" under specific stimulation, which is similar to the metabolic characteristics of brown adipose tissue - high energy consumption and heat production. Therefore, if the white adipose tissue can change the metabolic characteristics, it tends to "brown", will be expected to play a therapeutic effect.

More recently, Prof. Anutosh Chakraborty from the Scripps Research Institute (University of Florida) found a target protein, hexose inositol phosphokinase 1 (IP6K1), which is expected to be used to achieve this effect. Using recombinant rat proteins, they found that IP6K1 itself can affect the metabolic pathway of fat cells regulated by AMPK, which slows down the decomposition and consumption of fat in the body, thus accelerating the accumulation of fat. The results were published in the recent issue of The Journal of Clinical Investigation.

"We found IP6K1 to be a suitable therapeutic target for obesity and type 2 diabetes," said Professor Chakraborty. "We also found that TNP, an inhibitor of IP6K1, alleviates dietary-induced obesity and insulin resistance."

IP6K1 may have a significant effect on the metabolic pattern of white adipose tissue. Its substrate phytate (IP6) promotes AMPK phosphorylation, thereby upregulating PGC1α transcription coactivator and uncoupling protein 1 (UCP1) -mediated thermogenesis in promoting white adipose tissue browning. IP6K1 converts IP6 to inositol hexaphosphate (5-IP7), which no longer activates AMPK, and it inhibits Akt kinases that promote browning at the same time.

Mouse experiments show that cold stimulation can reduce the white adipose tissue IP6K1 levels, thereby increasing the decomposition of fat at this time of heat. When IP6K1 was knocked out in white adipose tissue, the activity of AMPK was increased, and the heat of lipolysis was enhanced significantly. The white adipose tissue showed browning characteristics, including the elevation of browning marker proteins such as UCP1 and PGC1α. When this IP6K1 knockout mouse received a high-fat diet, the propensity to develop obesity and insulin resistance was significantly reduced. The researchers further found that IP6K1 inhibitor TNP in mice can play a similar effect.

"In addition, TNP also promotes weight loss in mice and improves metabolic markers in obese mice," said Professor Chakraborty. Flarebio offers recombinant proteins such as recombinant App at competitive prices.

The relationship between ecotourism and wildlife

More and more tourists are willing to vacation in far-flung places around the places where they can use their money to make a positive impact on local people and local wildlife. However, researchers published a report in Trends in Ecology & Evolution on October 9th showed that the interactions between wild animals and friendly ecotourists eager to snap their pictures may unintentionally put animals at greater risk of being eaten. The research was conducted using recombinant horse proteins.

It is obvious that ecotourism business is booming these years. "Recent data showed that protected areas around the globe receive 8 billion visitors per year; that's like each human on Earth visited a protected area once a year, and then some!" said Daniel Blumstein of the University of California, Los Angeles. "This massive amount of nature-based and eco-tourism can be added to the long list of drivers of human-induced rapid environmental change."

The report shows the viewpoint that when animals interact with humans in benign ways, they may lower their guard. As they get used to staying with humans in comfortable environment, they may become bolder in other situations. It is difficult for them to recognize real predators.

Ecotourism is actually similar to domestication or urbanization. In all three cases, regular interactions between people and animals may lead to habituation. This is another kind of taming. A process that results from evolutionary changes but also from regular interactions with humans happens: domesticated silver foxes become more docile and less fearful. Domesticated fish are less responsive to simulated predatory attacks. Fox squirrels and birds that live in urbanized areas are bolder. It takes more to make them flee.

Besides, the presence of humans can also scare off natural predators, which creates a relatively safe environment for the smaller animals which could have become bolder. When humans are around, for example, vervet monkeys have fewer run-ins with predatory leopards.

The researchers hope more research on the interactions of humans with wildlife can be stimulated by this research. It will help people understand how different species and species in different situations respond to human visitation and under what conditions human act may put these species in danger situation. Flarebio provides good-quality recombinant proteins such as recombinant colec12.

Complex research identifies 238 genes that increase the lifespan of yeast cells

After ten years' exhaustive research, scientists at the Buck Institute for Research on Aging and the University of Washington have identified 238 genes that, when removed, increase the replicative lifespan of S. cerevisiae yeast cells. The results provide new genomic targets that could eventually be used to improve human health. The study was published online on October 8th in the journal Cell Metabolism, which also publishes other studies on recombinant human proteins.

"This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is," said Brian Kennedy, PhD, lead author and the Buck Institute's president and CEO. "It also sets up a framework to define the entire network that influences aging in this organism."

The Kennedy lab cooperated with Matt Kaeberlein, PhD, a professor in the Department of Pathology at the University of Washington along with his team. They began the complex process of examining 4,698 yeast strains, each with a single gene deletion. In order to determine which strains yielded increased lifespan, they counted yeast cells, logging how many daughter cells a mother produced before it stopped dividing.

"We had a small needle attached to a microscope, and we used that needle to tease out the daughter cells away from the mother every time it divided and then count how many times the mother cells divides," said Dr. Kennedy. "We had several microscopes running all the time."

All the eeforts brought back a lot of important information about how different genes, and their associated pathways, modulate aging in yeast. When deleting a gene called LOS1, it came out particularly stunning results. LOS1 helps relocate transfer RNA (tRNA), which bring amino acids to ribosomes to build proteins. It is influenced by mTOR, a genetic master switch long associated with caloric restriction and increased lifespan. And LOS1 influences Gcn4, a gene that helps govern DNA damage control.

"Calorie restriction has been known to extend lifespan for a long time." said Dr. Kennedy. "The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes."

The team also identified a number of the age-extending genes found in C. elegans roundworms, indicating these mechanisms are conserved in higher organisms. Many of the anti-aging pathways associated with yeast genes are maintained all the way to humans. The researchers hope this comprehensive and painstaking research can result in new therapies. Flarebio offers recombinant proteins of good quality such as recombinant colec12 at competitive prices.

To control bacterial growth through some new protein factors

It is well-known by those biochemists that crucial cell processes depend on a highly regulated cleanup system known as proteolysis, where specialized proteins called proteases degrade damaged or no-longer-needed proteins. According research using recombinant dog proteins, these proteases must destroy their own targets but not damage other proteins. However, the process is still not very clear to the in many cases.

Recently, researchers in Peter Chien's group from the department of biochemistry and molecular biology at the University of Massachusetts Amherst report that they have found how an essential bacterial protease controls cell growth and division. You can read the details in the current issue of Cell.

The lead author of the report is Kamal Joshi, a doctoral candidate in the Chien lab. He conducted experiments in the model bacterium Caulobacter crescentus. In this species, the ability to grow and replicate DNA is regulated by ClpXP, a highly conserved protease that in many bacteria allows them to cope with stressful environments such as the human body. Understanding how ClpXP is controlled could open a path to antibiotics that inhibit harmful bacteria in new ways.

How proteolysis controls Caulobacter growth is still a secret in the field. It is strange that ClpXP only destroys its target proteins at a specific time. They think there must be a factor they've ignored. There are some genetic evidence pointing to certain additional proteins, but no more details are discovered.

The lab purified all available proteins and designing experiments to query how they interacted and what functions were affected in their presence or absence. They found that the ClpXP protease could not by itself destroy the target proteins, and the additional regulatory proteins they had detected were controlling different parts of the process.

Later, they found these newly identified regulatory adaptors worked in a step-wise hierarchical way. The first adaptor was directly responsible for degrading a handful of proteins, but it could also recruit an additional adaptor that would deliver a different set of proteins and bind even more adaptors. Working with the Viollier lab from the University of Geneva, Switzerland, the researchers found scores of additional protease targets that were destroyed in this hierarchical way.

It is believed that this new fundamental knowledge may offer an entirely new target for developing new antibiotics with a high potential to avoid triggering drug resistance, because new compounds could be devised which would not simply target all bacterial growth, but only a specific pathway, such as virulence.

You don't force the benign bacteria to develop resistance in this approach because their growth isn't threatened. The hope is to target only those pathogenic organisms that are trying to overcome the stressful environment inside the human body. Though the researchers haven't known if these adaptor factors are common among all bacteria, but they decide to figure out. Flarebio provides recombinant proteins including recombinant Insr at great prices.

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.

Nanotechnology is expected to be used to treat Alzheimer's disease

Researchers have developed a new treatment that uses tiny droplets of fat to carry drugs into the brain to prevent the development of Alzheimer's disease. This method of treatment for targeting drugs to cancer cells has been successfully applied to memory loss in the first recovery of Alzheimer's disease in mice. The study, led by researchers at the University of Lancaster, was funded by the Alzheimer's Society and published in the journal Nanomedicine Nanotechnology, Biology and Medicine, which has published a lot of studies on recombinant human proteins.

This treatment uses tiny fat droplets known as nano-liposomes which are coated in protein fragments. It can prevent the amyloid from accumulating into plaques even at the condition of low concentrations. Amyloid plaques are toxic clumps of proteins that cause damage to cells in the brain of Alzheimer's patients. Mice that were genetically altered to develop Alzheimer's disease were injected with nano-liposomes for three weeks. Those who received the drug restored their long-term memory and were able to recognize the familiar object after 24 hours. In contrast, placebo-injected mice didn't have memory of the objects seen in previous day.

"The research results of this summer show a new discovery of antibody drugs that target amyloid plaques using the body's immune system," said lead investigator David Allsop. However, if these methods are successful, treatment must be instilled through the IV at the clinic and may have some potentially harmful side effects.

Commenting on the innovative approach to dementia treatment, Dr. Doug Brown, Director of Research and Development for Alzheimer's Disease, said, "There were no new dementia drugs in the last 15 years, and we are at a critical moment in dementia research. Crucially, we will continue to sniff new drugs into the brain approach. Although we look forward to the results of ongoing clinical trials, Alzheimer's Association will continue to finance innovative research to address dementia.

Nanotechnology is expected to bring enormous benefits to many people with different types of cancer. It is exciting that it can provide the same hope for the most common forms of dementia one day. Flarebio provides good-quality recombinant proteins like recombinant CDH11.

c-tau protein levels in people with early-onset psychosis are higher than healthy people

A study published in the International Early Psychosis Association (IEPA) in Milan, Italy, showed that c-tau protein levels in people with early-onset psychosis (onset earlier than 18 years) are significantly higher than those of healthy people. The conclusion was reached through a series of research using recombinant rat proteins.

Early onset psychosis (EOP), including early onset of schizophrenia (EOS) and emotional non-schizophrenia mental disorders, is a severe mental illness with the onset time before the age of 18, and the cause of EOP is not currently clear. Previous studies have shown that these patients often have severe neurological loss, such as inattention, lack of executive capacity and memory loss. The researchers believe that these symptoms show neurocognitive loss of the patients.

In diseases related to the loss of neurocognitive ability, such as Alzheimer's disease, deterioration is often associated with increased levels of neurodegenerative biomarkers such as tau proteins in blood and cerebrospinal fluid. In this study, the researchers analyzed plasma tau levels (including tau total protein [t-tau] and ruptured tau protein [c-tau] in EOP patients, these marks are related to dementia and trauma brain injury.)

The researchers analyzed plasma t-tau and c-tau levels in 20 patients and the control group (n = 20). The results showed a significant increase in c-tau levels in patients with an average of 2150 pg / ml in EOP compared to an average of 1100 pg / ml in the control group.

"This study shows that tau protein metabolism may affect EOP," the researchers conclude, "This study provides new insights into the pathogenesis of EOP as well as new therapeutic strategies." Flarebio offers good recombinant proteins such as recombinant CDH12 at competitive prices.

MDM2 proto-oncogene has an alarming and important function that promotes MYCN proto-oncogene expression

Scientists at the Sabang Institute at the Children's Hospital of California have recently discovered that the MDM2 proto-oncogene has an alarming and important function that promotes MYCN proto-oncogene expression. The study was published on October 17 on Oncogene, which also published some other studies on recombinant human proteins.

Retinoblastoma is a retinal neoplasm in children 1 to 2 years old. Although the incidence is low, if not treated, it can cause fatal or blinding serious consequences. This tumor also plays a special role in the study of cancer because its lesion progression is found to be associated with mutations or deletions of a single gene, RB1.

The MDM2 gene has been thought to be involved in the development of tumors because it promotes the transformation of normal cells into cancer cells. This function is thought to be associated with a tumor suppressor protein p53 that inhibits apoptosis which leads to aberrant proliferation.

MDM2 also plays an important role in other p53-independent signaling pathways. This protein, called MYCN, is regulated by MDM2 and plays an important role in cell proliferation. In the presence of this protein, retinoblastoma can grow by 20% to 25%, leading to secondary disease and poor prognosis. Although MYCN has the potential to be a therapeutic target, it is difficult to be blocked by a single small molecule. The findings of this study provide the theoretical support for the regulation of MYCN expression by targeting MDM2.

This study first elucidates that retinoblastoma is more dependent on MDM2 than on MDM4 which is another member of this family. Flarebio offers recombinant proteins of good quality such as recombinant CDH4 at competitive prices.

Alzheimer's disease of experimental mice is curable now!

Molecular biologists have successfully created and tested the first reverse transcriptase therapy for Alzheimer's disease by use of recombinant mouse proteins, which protects mice from disease. The study was published in the Proceedings of the National Academy of Sciences (PNAS).

"Our results show that gene therapy can be used to treat Alzheimer's disease, although it is too early to talk about this. Therefore, we must overcome a large number of obstacles. In addition to direct injection of brain, we can't induce this gene therapy through other methods," said Magdalena Sastre at the Imperial College in London, UK.

In the last two years, biologists have gained a better understanding of the causes of Alzheimer's disease and the definition of the disease. For example, recently scientists have found that Alzheimer's disease may be transmitted; β-amyloid plaques may be an important part of the innate immune system; and some therapies that are expected to treat the disease.

One approach - forcing the PPARGC1A protein associated with cell self-purification systems and cellular metabolic work to actively counteract beta-amyloid plaques. Sastre and colleagues believe that this process can be achieved by gene therapy (embedding other copies of the gene in hippocampal cells, storage centers, and the cerebral cortex). To test this idea, the scientists grew a population of mice with Alzheimer's disease and introduced a special retrovirus that contained other copies of the PPARGC1A protein in their brains. Another group of uninfected rodents was the control group.

Four months later, scientists compared the state change of the two groups of rats. It was found that the presence of a copy of the PPARGC1A protein had a very positive effect on rodent status, significantly reducing the amount of beta-amyloid protein entanglement in the rat nerve cells and preventing the negative effects produced by the development of Alzheimer's disease.

According to scientists, these mice have good memory, and they complete the task of finding a maze outlet and the ability to deal with other cognitive problems as much as not suffering from Alzheimer's disease in healthy rodents. The fact that rodents are healed proves that almost no cell survives in the hippocampus and cortex. When Alzheimer's disease enters the final stage, neurons usually die in large numbers.

Scientists hope their research will serve as the basis for the development of retroviral vaccines that can be adapted to humans without the need to inject potentially lethal drugs directly into the brain. According to scientists, this gene therapy can not only adapt to the existing Alzheimer's disease, but also can be used as a special vaccine to prevent disease development. Flarebio offers good-quality recombinant proteins such as recombinant ITGB2 at good prices.

The protein which leads to Alzheimer's disease

A study published in the issue of Molecular Psychiatry on October 18th suggests that specific proteins with cognitive decline in Alzheimer's disease also play a role in schizophrenia. This means that a drug of target protein can treat a variety of neuropsychiatric disorders.

Researchers at Yale University have been studying the role of synapses in brain cells by recombinant mouse proteins. Excessive amounts of STEP protein are found in the brains of human and animal models of Alzheimer's disease, Parkinson's disease, fragile X syndrome and schizophrenia. This increase leads to disruption of synaptic function, leading to cognitive impairment of these diseases.

In previous studies, he and colleagues had shown that reducing STEP or using drugs to suppress STEP is beneficial in reducing cognitive impairment in Alzheimer's disease mice. In addition, they also found that a high level of STEP content was found in the stem cells obtained from the skin of two groups of patients with schizophrenia. For these biochemical and electrophysiological abnormalities of human stem cell cells, STEP inhibitors were administered.

Although early drug trials of Alzheimer's disease have proved difficult to be developed for clinical use, Professor Rambus and colleagues at Yale University are developing an inhibitor. If successful, this study may be of more practical therapeutic value. Flarebio offers good-quality recombinant proteins such as recombinant ECE1.

Researchers from Tsinghua University find that Hsp90α can detect liver cancer

Tsinghua University held a press conference on the 19th, saying that the Luo Yongzhang team confirmed that the tumor marker of heat shock protein 90α (Hsp90α) can be used for liver cancer patients using recombinant human proteins in the world for the first time, and the kit has been approved in clinical by the State Food and Drug Administration.

At present, most of the liver cancer patients have been found in middle and advanced stage. Then it is difficult to treat, and the survival is generally poor. The most commonly-used marker for liver cancer is alpha fetoprotein (AFP), but the sensitivity is only about 50%. Luo Yongzhang said that the new liver cancer marker Hsp90a breaks through the limitations of AFP and has a high sensitivity to hepatocellular carcinoma, intrahepatic cholangiocarcinoma, mixed liver cancer and other common types of liver cancer, having great significance for the comprehensive improvement of liver cancer prevention and treatment and reducing liver cancer mortality.

According to Luo Yongzhang team's findings, in patients with negative HCC the AFP test results, the detection rate of Hsp90α is 94%, which proves that Hsp90α is the world's most superior performance of liver cancer markers.

According to reports, the kit not only can detect lung cancer but also can detect liver cancer. As early as 2013, Luo Yongzhang team proved that plasma Hsp90α is a new tumor markers through clinical trials of lung cancer in the world for the first time, and it has been widely used in medical institutions.

Heat shock protein is a kind of protein with molecular chaperone function in cell. Hsp90α is an important member of the heat shock protein family. It is widely distributed in the cells from microbes to mammals and plays an important role in maintaining cell homeostasis. The research results will significantly improve the early detection level of liver cancer and save people from the fear of liver cancer and have a global impact. Flarebio offers good-quality recombinant proteins such as recombinant CDH15 at competitive prices.

Get to know the greatest athlete in the world!

When speaking of the greatest athletes in the world, you may think of the names like Usain Bolt or Yohan Blake generally. It's amazing that scientists now find the greatest athletes may be the in the water and covered in scales through study using recombinant proteins - They are fish.

They discovered that fish are far more effective at delivering oxygen throughout their body than almost any other animal. This advantage gives them the athletic edge over other species.

"Fish exploit a mechanism that is up to 50-times more effective in releasing oxygen to their tissues than that found in humans," says study lead author, Dr Jodie Rummer from the ARC Centre of Excellence for Coral Reef Studies at James Cook University.

Haemoglobin in fish, the protein in blood that transports oxygen, is more sensitive to changes in pH than ours and more than the haemoglobins in other animals. It is quite important for fish during times of stress, to escape from predators, or when they are living in water that is low in oxygen. They can double or even triple oxygen delivery to their tissues during these critical times.

In the last decade, researchers have been using rainbow trout to investigate oxygen delivery in fish. They first discovered and tested this mechanism by monitoring muscle oxygen levels in real-time in trout. Now they have determined just how powerful that system can be and have compared the results with medical studies on humans.

It shows us how fish have adapted this very important process of getting oxygen and delivering it to where it needs to be so that they can live in all kinds of conditions such as warm or cold water, or nd water with high or low oxygen levels. For these athletic fish, enhanced oxygen delivery may be the most important adaptations during their long evolutionary years. Flarebio provides good-quality recombinant proteins like recombinant NRG3 at competitive prices.

Researchers develop a platform to recognize specific target antibodies

A new study may completely change the slow, cumbersome and expensive process of detecting the antibodies that can help with the diagnosis of infectious and auto-immune diseases such as rheumatoid arthritis and HIV. An international research team has made use of recombinant proteins including recombinant human proteins to design and synthetize a nanometer-scale DNA "machine" whose customized modifications enable it to recognize a specific target antibody. This new approach is said to support the development of rapid, low-cost antibody detection at the point-of-care, eliminating the treatment initiation delays and increasing healthcare costs associated with current techniques.

The binding of the antibody to the DNA machine causes a structural change which generates a light signal. The sensor does not need to be chemically activated and is rapid - in five minutes - enabling the targeted antibodies to be easily detected, even in complex clinical samples such as blood serum.

This DNA nanomachine is highly versatile that can be in fact custom-modified so that it can detect a huge range of antibodies, this makes our platform adaptable for many different diseases.

The modular platform provides significant advantages over existing methods for the detection of antibodies. It may prove to be useful in a range of different applications such as point-of-care diagnostics and bioimaging.

Besides, this platform has an advantage of low-cost. The materials needed for one assay cost about 15 cents, which makes the approach very competitive in comparison with other quantitative approaches.

These preliminary results make the researchers exciting. There are more to make this approach available to everyone. Flarebio offers recombinant proteins of good quality like recombinant ACSL3 at good 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.

Scientists find the new way of tobacco smoke inducing cancer

A recent study by researchers at the University of Kentucky revealed a new way of tobacco smoke inducing lung cancer: inhibiting the DNA repair process, which is called nucleotide excision repair (NER). The results were published in the journal PLoS ONE. Many constituents of tobacco smoke are carcinogens that can damage DNA. This damage must be prevented by the DNA repair process to further eliminate the genetic mutation process. In this way, researchers found through recombinant human proteins that DNA repair processes such as nucleotide excision repair are critical to block the accumulation of the final DNA mutation, which drives the development of lung cancer.

"It has been determined that carcinogens in tobacco smoke can cause mutations," says Isabel Mellon, an associate professor and principal investigator in the Department of Toxicology and Cancer Biology, but only a handful of researchers have investigated the effects of tobacco smoke on DNA repair pathways influences.

Mellon and her team studied the effects of cigarette smoke concentrates (CSC), a commonly used alternative to tobacco smoke, on the nucleotide excision repair process in cultured human lung cells. They found that the addition of CSC to these cells significantly reduced nucleotide excision repair efficiency. In addition, the researchers showed that the addition of CSC stimulated the destructive nature of a key nucleotide excision repair protein called XPC. The abundance of XPC reduction can then explain how the CSC inhibits the nucleotide excision repair process.

The results indicate that tobacco smoke has a dual effect on DNA integrity: it not only impairs DNA but also inhibits the critical process of repairing DNA damage. "Inhibition of nucleotide excision repair may increase the risk of mutation and cancer, particularly in the case of chronic DNA damage induction, such as in smokers' lung problems," Mellon explained.

If this is the case, the ability of repair damaged DNA in lung cells of a given human can be used to predict the risk of lung cancer in that person due to tobacco smoke. "In the future, we want to determine how different the efficiency of the nucleotide excision repair pathway varies among people," Mellon said. "We are also continuing to study how the efficiency of human DNA repair is adversely affected by environmental factors. Whether due to genetic factors or environmental factors, reduce of DNA repair will increase the risk of cancer patients." Flarebio offers recombinant proteins of good quality such as recombinant Cdh10 at competitive prices.

Why do plant twists and turns happen?

With the rapid growth of the population, crop producers have to grow crops in more challenging terrain where plant roots would be faced with barriers. Under the circumstances, physicists at Cornell University and plant biologists from Boyce Thompson Institute have uncovered a valuable plant root action. When the roots' downward path is blocked, as often happens in rocky soil, it will display a "grow and switch" behavior. The finding is published in the latest Proceedings of the National Academy of Sciences, which also published some other studies on recombinant proteins.

The research group observed growth patterns arising from how plant roots cope with limitations of their gravity sensors. When there is no root barrier, its growth is straight down. On the contrary, when barriers are present, roots coil in some instances and wave in other situations.

"We found that the roots make planar coils when the barrier they encounter is flat, and transition to wavy geometry when the barrier is at an angle," said Tzer Han Tan '14, lead author on the new paper, "How Grow-and-Switch Gravitropism Generates Root Coiling and Root Waving Growth Response in Medicago truncatula."

Plant roots have gravity sensors in each cell at the root's tip, which are comprised of dense particles called "statoliths" that enable the roots to determine which way is down. When a root meets a barrier, the root conquers the barrier with a search strategy. Surprisingly, the strategy the plants adopt is basically the same search algorithm as the 'run-and-tumble' strategy found in many bacteria. Essentially, the roots grow in a particular direction, and from time to time curve to switch their growth directions. The researchers learned that these course corrections have a 90 percent accuracy.

There is no doubt that the detail knowledge of how roots grow is critical for more efficient food production in the future. Only knowing more can we deal with the problems brought by climate changes. Flarebio provides superior recombinant proteins like recombinant Insr at good 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.

Japanese use in-vitro light to control DNA recombinant reaction

The University of Tokyo in Japan announced on October 11th in 2016 that they have successfully developed a new technology which can efficiently control the DNA recombination reaction by conducting short-term exposure to weak light and using recombinant horse proteins.

Associate Professor Okazaki Yasuke, Associate Professor Takashi Sato from Graduate School of Comprehensive Cultural Studies, the University of Tokyo and Professor Yazawa Shinya of the Department of Rehabilitation and Rehabilitation Medicine of Columbia University, Yasuyuki Yasuo, and other researchers have completed the related research. Specific results have been published in the October 10th issue of the well-known US scientific journal Nature Chemical Biology.

Cre-LoxP recombinase system technology is used by most researchers to knock out the base sequence of a target gene from the genome or to insert a gene into the genome. In recent years, the use of compounds and light to artificially control the Cre-LoxP recombinase system has attracted more and more attention. In particular, if the Cre-LoxP recombinase system can be controlled by light, then targeting specific tissues and cells at any time point to induce DNA recombination will be realized. However, the existing technology uses light control but the efficiency of DNA recombination is significantly reduced, which is a major problem consistent with the researchers.

In this study, the panelists connected light-activated protein recombinase (Cre) which was temporarily inactive and successfully developed a light-activated Cre recombinase that controls the recombination of DNA by light-ray irradiation. The enzyme was named PA-Cre. PA-Cre is capable of producing light recombination with very low light (one hundred thousandth of the light intensity commonly used in light genetics) and a short time of about 30 seconds is enough to induce DNA recombination. In addition, the researchers have successfully used PA-Cre to conduct DNA recombination on the selected target site.

On this basis, the researchers applied PA-Cre to the genetic gene in the deep of mouse body to conduct light control. It has been found that the use of a non-invasive method for light irradiation from the outside of an organism can induce DNA recombination efficiently in the liver of a mouse's deep part of the body. The researchers said that the results enable the genetic activities within the living body can be controlled by non-invasive light irradiation, which is of great significance in proving the function of the disease-related gene. Flarebio offers good-quality recombinant proteins like recombinant CDH11 at competitive prices.

New CRISPR tool has been released by Chinese scientists

Recently, the international academic journal Nature Methods published the latest research results of the Targeted AID-mediated mutagenesis (TAM) enablesefficient genomic diversification in mammalian cells by the Changxing Research Group of the Shanghai Institutes for Biological Sciences / Shanghai Jiaotong University School of Medicine and Institute of Health Sciences. They combined activation-induced cytidine deaminase (AID) with CRISPR-dCas9 and used recombinant mouse proteins to create an effective genetic diversity tool for high-throughput screening of functional variants. This is a new method of DNA Base editing which is efficient and high-throughput.

Inspired by the "mutant self" mechanism and under the guidance of researcher Chang Xing, Dr. Ma Yunqing and Zhang Jiayuan discovered that when the nucleosidase-deficient Cas9 protein and the cytosine deaminase AID that induced antibody high-frequency mutation were fused, cytosine and guanine can be random to the other three bases on sgRNA-targeted genomic DNA. This new method can be specific to the cell DNA sequence diversity, the completion of genetic screening so as to analyze single nucleotide mutations function. At the same time, under the assist of a peptide inhibitor, dCas9-AID can induce specific cytosine to thymidine conversion to achieve precise editing of single base. The researchers used dCas9-AIDx to target BCR-ABL in chronic myelogenous leukemia cells, which effectively identified known mutations and new mutations that confer resistance to imatinib. Studies have shown that dCas9-AID is a very useful genetics tool and can screen functional acquired variation at the single-base level.

The team further demonstrated that this approach could rapidly and effectively mimics the heterogeneity of drug resistance in tumor cells, predict possible mutations in drug resistance, thus improving small molecule inhibitors and studying interaction of small molecules and protein targets. The results of the study provide a new approach of analysis of gene regulatory elements at the level of molecular evolution, gene therapy and single base level. Flarebio offers recombinant proteins of good quality such as recombinant CDH12 at good prices.

This herbal ingredient is effective on a certain kind of leukemia

An international study group led by the University of Hong Kong reported in a new issue of the journal Science Translational Medicine that the effect was significant when homoharringtonine extracted from the genus Cephalotaxus was used to treat acute myeloid leukemia patients with FLT3-ITD gene mutations. Acute myeloid leukemia is a common cancer of the adult human blood system, and nearly 30% of patients with acute myeloid leukemia carry FLT3-ITD gene mutations.

Liang Ruhong, vice president of the Li Ka-shing School of Medicine of the University of Hong Kong said that the standard chemotherapy regimen and drug sorafenib were not effective in patients with acute myeloid leukemia carrying the gene mutations. In order to find a better treatment, they made use of leukemia cells of patients and recombinant rat proteins to conduct drug screening in vitro and found that homoharringtonine has significant inhibition function on it.

According to Liang Ruhong, homoharringtonine is a bio-ester base derived from the Cephalotaxus plant. In China, homoharringtonine is commonly used in the treatment of acute myeloid leukemia but not for a specific type of leukemia, so the effect is not so significant.

Liang Ruhong and his colleagues recruited 24 acute myeloid leukemia patients who showed relapse or are refractory with FLT3-ITD gene mutations to conduct clinical trials. They used homoharringtonine and sorafenib to conduct combination therapy, and finally 20 patients Leukemia cells in vivo were removed, and the overall survival was significantly longer.

Liang Ruhong said, "Homoharringtonine can inhibit cell protein synthesis so that cancer cells can't produce important proteins, leading to cancer cell apoptosis. Relative to the current approach, the side effects of combination therapy are small and can be applied to frail or elderly patients." Liang Ruhong thought that this study provides an effective treatment strategy for FLT3-ITD acute myeloid leukemia. Flarebio offers superior recombinant proteins such as recombinant ITGB2 at great prices.

Abnormal protein deposition is linked with incidence of cognitive dysfunction disease

IPS Cell Research Institute of Kyoto University, Japan, announced that they successfully used cells from patients with frontal lobe degeneration and recombinant human proteins to produce iPS cells (induced pluripotent stem cells), confirming the abnormal protein deposition is associated with the incidence of cognitive dysfunction disease.

The team led by Prof. Inoue Takeuchi, director of the Institute of iPS Cell Research, completed the experiment. The results were published in Scientific Reports in UK on October 10, 2016.

Frontotemporal lobar degeneration (FTLD) is a disease caused by social disorders and language disorders due to focal cerebral frontal and temporal lobar degeneration and atrophy. Experts generally believe that Tau gene mutation is the cause of frontotemporal lobe degeneration, but the specific mechanism has not been proven.

The researchers used the cells of two patients with two different types of Tau gene mutations to produce iPS cells and then used gene editing technology to modify the gene mutation of iPS cells. They transformed the iPS cells of these two people into neurons cells and compared them, finding that Tau gene mutations may cause the deposition of abnormal proteins.

In addition, the researchers also found that in iPS cells of Tau gene mutations, the calcium content increased. If inhibiting calcium ions into the cells, then the amount of abnormal protein can be reduced and cell survival rate can increase. Professor Inoue Haruhisa said, "This achievement is an important step towards new drug research and development." Flarebio offers recombinant proteins of good quality such as recombinant ITGB2 at great prices.

The new strategy of screening venom peptides aiming at ion channel

The ion channel is an important drug target of pain, autoimmune diseases, tumor and other diseases. The toxin polypeptide of animals is formed in the evolution of hundreds of millions of years, and it is rich in active ion channels. There is an urgent need to find a way to quickly discover toxin peptides aiming at ion channels.

Professor Richard Lerner from the Institute of Immunochemistry of the Shanghai University of Science and Technology (SIAIS) has innovatively proposed an autocrine-based screening method to screen high-throughput peptides for ion channels. The researchers first constructed a set of signaling systems based on autoadhesive detection of ion channels binding to the toxin polypeptide and using recombinant mouse proteins. In this system, the toxin polypeptide can be anchored to the cell membrane by the platelet-derived growth factor receptor transmembrane domain PDGFR-TM and is fused to the TEV protease at the intracellular end of the transmembrane domain. The ion channels are linked to the artificial transcription factor GAL4-VP16 by the TEV protease substrate sequence. TEV protease cleaves its substrate to release GAL4-VP16 and activates the expression of fluorescent protein reporter gene when it binds to the toxin polypeptide. Fluorescent protein-expressing cells can be sorted by flow cytometry.

Using this method, the researchers screened a library of 589 virulent polypeptides for ion channel Kv1.3. They found that 25 of the 27 enriched toxin polypeptides that were the most enriched in the screening were known as Kv1.3 blocker, and their experiments confirmed that the Clltx1 polypeptide from scorpion venom was a novel and highly effective Kv1.3 antagonist. The system further reconstructed the ShK protein from the sea anemone toxin and constructed nearly one million ShK analogues with long-acting properties for screening. The screened ShK analogues showed high Kv1.3 antagonistic potency and no off-target effects on a series of ion channel molecules which are highly similar to Kv1.3. Flarebio offers superior recombinant proteins such as recombinant App at good prices.

Mice study shows that autism is linked with gene variation

Autism is a mental illness of high incidence, and the incidence rate is 2%. On its pathogenesis, it is generally considered to be fetal neurological developmental disorder, but the specific mechanism has been a puzzle. In recent years, a large number of genetic mutations have been carried out in autism patients, and by using recombinant human proteins, it is found that the highest proportion of mutations is CHD8, which controls changes of chromosome structure.

Researchers at the Institute of Biological Defense Medicine, Kyushu University, Japan, have been leading the world in the research of CHD8. In a recent experiment, they found that when the genes of mouse show the same variation, there will be communication abnormalities, stubborn temper and other human autism characterization. Studies have shown that due to genetic variation, the number of proteins produced by this gene is reduced and that other proteins called "REST" are abnormally active, leading to neurodevelopmental retardation.

For CHD8 gene derived from the father or CHD8 gene from the mother in autistic patients, the phenomenon of "semi-loss", i.e. a party gene lack happens often. The research team created mice that turning this gene into a "semi-defective" model and observed them. They found that mice showed increase of uneasiness and abnormal communication which were similar to the symptoms of human autism. The brain of the mice was analyzed, and the results showed that the activity of REST increased abnormally.

A further study of autism mice using the TransOmics system showed that a decrease in the amount of CHD8 due to genetic variation could lead to a high degree of activation of the neurotrophic protein REST, leading to neurodevelopmental delay. That is, if the amount of CHD8 is increased by the administration of human factors, or taking measures are taken to inhibit the activity of REST, it may be possible to find a way to treat autism.

The study was published in the British scientific journal Nature on the electronic version in September 2016. Flarebio offers recombinant proteins of good quality such as recombinant ECE1 at good prices.

New method of treating heart failure is coming

When the heart can't provide enough blood to maintain the body needs and show systolic and diastolic dysfunction, it will show heart failure. Heart failure is a common age-related disease in an aging society, and it is often with poor prognosis.

Ouchi et al from Kumamoto University found through recombinant rat proteins that age and hypertension and other factors will bring a burden on myocardial cells, and myocardial cells secreted by a protein - promote angiogenesis factor protein-like protein 2 will increase. This protein will weaken the regulation of calcium concentration in cardiac cells and other functions, causing decrease of myocardial contractility and triggering heart failure.

The researchers used gene knockout technology to breed mice that couldn’t produce the protein and found that the mice were not as susceptible to heart failure as normal mice. The study also found that moderate exercise can reduce the level of pro-angiogenic factor-like protein 2, helping to prevent heart failure.

The paper was published in the online edition of the journal Nature. The researchers pointed out that in the future, gene therapy can inhibit levels of myocardial angiogenesis factor protein-like protein-2, thus treating heart failure. Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. It provides you with good-quality recombinant proteins including recombinant App at great prices.

Scientists find new target to treat chronic kidney disease

Renal fibrosis is a common pathophysiological change of chronic kidney disease. It can lead to renal failure, and there is no better treatment. Dr. Ian Logan from the University of Newcastle, UK, and his colleagues conducted a study of epigenetic modulators through recombinant human proteins, including SETD7, to determine whether epigenetically modulating factors are potential therapeutic targets for chronic kidney disease. The results were published in the Lancet.

The researchers used human kidney fibroblasts, mesangial cells, and mouse embryonic fibroblasts to analyze fibroblast transformation, extracellular matrix protein expression (immunofluorescence, wound healing), and whole-gene expression (whole genome chip technology) levels. The interaction of the lysine methyltransferase SETD7 with SMAD3 (immunoprecipitation), SMAD3 stability, and SMAD3 nuclear import was analyzed using renal tubular epithelial cells.

The results show that Transforming growth factor β1 (TGFβ1) -induced myofibroblast transformation was not found in SETD7-deficient cells. In addition, SETD7 lacks fibroblast collagen concentration and fibronectin - 1 concentration was lower than SETD7 normal cells, and wound healing slowed down. TGFβ1 can promote the interaction of SMAD3 with SETD7, thus increasing the stability of SMAD3 in cells. Immunofluorescence and subcellular separation revealed that SMAD3 nuclear input was dependent on SETD7. SETD7 overexpression increased the SMAD3 transcriptional activity of cis-regulatory elements (plasminogen activator inhibitor 1 and CAGA), while SETD7 deficiency can reduce SMAD3 transcriptional activity. Gene Ontology analysis showed that SETD7 regulates the expression of fibrogenic genes.

The study shows that SETD7 plays an important role in fibrogenesis - a major feature of chronic kidney disease and other fibrotic diseases. In view of the results of this study, drug inhibition of epigenetic regulators is expected to be a novel therapeutic approach for chronic kidney disease. Flarebio offers recombinant proteins of good quality such as recombinant ECE1 at competitive prices.

A protein that plays an important role in the development and progression of cancer

Researchers at the Sylvestre Cancer Research Center in the United States have discovered a protein that plays an important role in the development and progression of cancer through research using recombinant dog proteins, and this protein accumulates in dormant cancer cells and forms amyloid small body. Once this amyloid decomposition, cancer cells will be re-active. The study was published in the journal Developmental Cell.

We know that these amyloid bodies are related to the occurrence and development of Alzheimer's disease and Parkinson's disease, the relation of deposition of starch bodies and cancer is not clear. This study suggests that we can apply the knowledge of neuroscience to cancer so as to obtain a variety of types of cancer treatment.

"We found that these proteins are abundantly present in dormant cancer cell bodies, while the heat shock pathway breaks down the amyloid bodies formed by this protein deposition, which in turn restores dormant cancer cells," the experts said.

The study also found that ribosomal non-coding genes control the formation of amyloid bodies in cancer cells, so we can also take this gene as a target to produce drugs. If we can prevent the decomposition of amyloid in cancer cells, then we may be able to keep the cancer cells dormant indefinitely. In addition, we can also try to find another way for cancer cells to produce such amyloid bodies, thus making the active state of cancer cells to dormant state.

Through this study, we can imagine in the future that we may not have to completely remove the cancer cells. We can just keep it in a dormant state. Experts say that they are confident they can develop a new kind of cancer drugs. These drugs take related genes and pathways as targets, and some related drugs have been put into the market, while other drugs are still in the research process. Flarebio provides good-quality recombinant proteins such as recombinant NRG3 at competitive prices.

New findings help to improve the development of anti-TB drugs

Tuberculosis (TB) caused by M. tuberculosis (Mtb) remains to be a major global public health challenge. TB research and new drug development are urgently needed due to the limited availability of drugs that are currently available to treat TB, especially MDR-TB and XDR-TB. Mtb is a typical intracellular pathogen. Mtb evolved a variety of immune escape strategies in the process of long-term coexistence and interaction with the host. Therefore, in-depth study of the interaction between Mtb and the host immune system using recombinant human proteins and its regulatory mechanism is of great significance for elucidating the molecular mechanism of Mtb latent infection and pathogenesis and providing new drug targets for the development of anti-TB drugs.

Liu Cuihua research group at The Institute of Microbiology has been working on the molecular mechanism of the interaction between Mtb and other important pathogens and hosts. In recent years, he has published a series of studies in Nature Immunology (2015), The Journal of Immunology (2015), etc., to uncover the new mechanism of Mtb regulating host cell function then escaping host innate immunity through secreting effect protein (including PtpA and Mce3E, etc.). In addition to investigating the role of effector proteins in the immune regulation of the host from the perspective of pathogens, the team explored the mechanisms of immune defense in pathogen infection from a host perspective. In the process of in-depth study of the regulatory function of the Mtb-effector protein PtpA, they identified host interaction protein TRIM27 (an ubiquitin ligase) of PtpA.

Further studies have shown that TRIM27 can act as a host restriction factor to inhibit the survival of mycobacteria in macrophages. TRIM27 can activate JNK / p38 signaling pathway of host cells and promotes apoptosis in ubiquitin ligase-dependent manner, thus inhibiting the intracellular survival of mycobacterium. Interestingly, the study also found that Mtb PtpA can bind to RING domain of TRIM27 protein to antagonise TRIM27-mediated activation process of innate immune signaling pathways and apoptosis in order to achieve the purpose of promoting intracellular survival of Mycobacterium. The study revealed the dynamic process and molecular mechanism of the interaction between pathogen and host, providing new ideas and specific targets for the development of antituberculosis drugs. Flarebio offers recombinant proteins of good quality such as recombinant ACSL3.

Low-density lipoprotein may be related to risk of diabetes

According to a study published in the Journal of the American Medical Association on Oct 4th, LDL lowering gene variants are associated with an increased risk of type 2 diabetes. The research was conducted using recombinant proteins such as recombinant mouse proteins.

Dr. Luca A. Lotta from the University of Cambridge, UK and his colleagues conducted heredity-associated meta-analysis to examine the association between low-density lipoprotein (LDL) reduced genetic variants and type 2 diabetes and coronary artery disease. The data included 50,775 patients with type 2 diabetes and 270,269 controls as well as 60,801 patients with coronary artery disease and 123,504 controls.

The researchers observed an inverse association between LDL-lowering of NPC1L1 gene variants and coronary artery disease (a predicted odds ratio of 0.61 for the gene predicts a reduction in LDL per 1 mmol / L), and they also discovered a direct association between type 2 diabetes mellitus (the predicted odds ratio of the gene for the reduction of LDL per 1 mmol / L was 2.42). For PCSK9 gene variation, the odds ratio for type 2 diabetes was 1.19 for every 1 mmol / L reduction in LDL. For a given reduction in LDL, the risk of coronary artery disease has similar reductions with gene mutation; type 2 diabetes mellitus isomer correlation was observed.

"In this meta-analysis, the presence of LDL-lowering NPC1L1 or nearby gene mutations was associated with a higher risk of type 2 diabetes," the study authors write. Flarebio provides you with good-quality recombinant proteins like recombinant Lrp3 at good prices.

The pathogenic protein of senile dementia may be used to treat cancer

For Alzheimer's disease, the existence of amyloid protein is often a bad predictor, because β-amyloid is a major constituent of senile plaques in the brain and is one of the most important indicators of disease severity, and it is also the key target for dementia immunotherapy.

However, as early as the end of May, in an article published in Science Translational Medicine, scientists conducted research using recombinant human proteins and speculated that β-amyloid may also carry an ancient evolution "mission": to protect brain from pathogen invasion and its function is similar to antimicrobial peptides.

In early October, scientists discovered "good" point for amyloid. The research team at the University of Miami Miller School of Medicine has revealed that amyloid allows can make cells including cancer cells to enter dormant state. This may bring new paradigm for cancer treatment. The related research results were published in the Cell sub-publication Developmental Cell on October 6th.

Dr. Stephen Lee led the research team to discover the formation mechanism of amyloid. Motif is the structural level of protein between the secondary structure and tertiary structure. Amyloidogenic motifs (ACMs) are able to direct amyloid production by interacting with non-coding ribosomal RNA (rIGSRNA). Β-amyloid peptide has a function similar to ACM, for it can mediate intracellular deposition of amyloid protein. In the signal pathway of heat shock, the key elements can degrade amyloid protein.

The researchers believe that this mechanism is one of the ways that cells respond to stress, allowing cells to store large amounts of proteins and enter the dormant state. Amyloid production allows cells to remain active under stress for extended periods of time. Dormant cancer cells would store large amounts of amyloid proteins, and heat shock signaling pathways will degrade the deposition of amyloid, making cancer cells "wake up", thereby promoting its proliferation and proliferation.

"If we can stop the degradation of amyloid in cancer cells, we will have the ability to keep the cancer cells dormant forever," Dr. Lee said. "In addition, we might be able to induce active cancer cells to store amyloid, thus making them dormant." Although this new idea can't eliminate cancer cells, it can block the deterioration of cancer. Flarebio offers recombinant proteins of good quality such as recombinant LRP3 at competitive prices.

A certain protein may be the starting factor for Alzheimer's disease

Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis all are likely to be related to structural collapse of the accumulation of proteins and brain inflammatory response. However, although there are many studies on recombinant rat proteins, the specific causes and mechanisms are unclear.

Researchers at the University of Louisville School of Medicine have found that proteins produced by intestinal bacteria can cause structural protein folding errors in the brain and inflammation of the brain. Their study found that intestinal bacteria can produce a protein has structure similar to the brain protein, and this protein will lead to an increase in the number of α-synuclein in the brain. In the brains of patients with Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, structural abnormalities of alpha-synuclein and associated amyloid accumulation can be found.

α-Synuclein is a protein existing in the brain of normal humans. In the brain of patients with Alzheimer's disease and Parkinson's disease, the protein will accumulate and form amyloid substances, thereby impairing brain function. Experts suspected that intestinal bacteria can produce a protein which can bring structural folding abnormalities of proteins in brain, and those brain proteins with abnormal structure will deposite in the brain. In addition, experts also suspected that the protein secreted by intestinal bacteria will promote the inflammatory response of brain.

A study implanted E. coli which can produce this protein in the intestine of experimental mice, while the other group of control mice was implanted with E. coli that could not produce the protein. The results showed that the experimental group mice brain produced more α-synuclein, and the brain inflammation was also stronger than the control group. There was a similar study on nematode also showed a similar result.

The expert said, "These two similar studies on different animals suggest that certain protein secreted by enteric bacilli may be the starting factor for Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Understanding this is very important, because many of these factors are not genetically determined. While coliform bacteria are part of our body, and we have many possible ways to influence the number of these bacteria, thereby treating the disease.

Colorectal bacteria play an important role in age-related brain degenerative diseases. Finally, experts said, "We are continuing our efforts to explore this mechanism, thus exploring further possible therapies." Flarebio offers good-quality recombinant proteins like recombinant CDH12 at competitive prices.

Yoshinori Ohsumi finds the real autophagy mechanism

The Nobel Prize in Physiology or Medicine in 2016 was awarded to Yoshinori Ohsumi who is interested in recombinant human proteins, because he discovered the autophagy mechanism. This is an evolutionarily conserved process in which eukaryotic cells can be partly recirculated through transporting double membrane vesicle to lysosome. Unlike other mechanisms of cellular degeneration, autophagy can remove aged or damaged proteins, macromolecular complexes and organelles, leaving place for participation in new physiological processes. In addition, autophagy is also a key cellular process for the removal of invading microbes and toxic protein aggregates, which plays a key role in the fight against infection, aging, and many human diseases.

Although autophagy has been confirmed in the 1960s, scientists still have little knowledge of its mechanisms and physiological significance over the next few decades. The work of Yoshinori Ohsumi significantly changes the understanding of this important cellular process.

In 1993, Yoshinori Ohsumi published his groundbreaking in fifteen genes in the yeast. Subsequently, he cloned these genes in yeast and mammalian cells and elucidated the function of the coded protein. Based on the pioneering discovery of Yoshinori Ohsumi, the importance of autophagy in human physiology and diseases is now widely recognized. Flarebio offers recombinant proteins of good quality such as recombinant Nrg2.