Researchers have found the key protein of leukemia

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

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

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

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

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

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

Scientists have discovered more in the processes of protein folding

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

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

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

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

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

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

A vaccine that would fight all mosquito-borne diseases

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

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

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

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

New cancer immunotherapy can kill target cancer cells

Researchers have developed a manual structure that can mimic cell membranes which can "open" immune cells and let it attack and destroy a specified target. According to research using recombinant horse proteins, this approach may be used as a cancer immunotherapy in the future, and it also provides a more in-depth understanding about how immune cells are activated to find and kill cancer cells. The results of the study were published recently at a joint meeting between the UK and the Dutch Society of Immunology. The meeting was held in Liverpool, England.

Immunotherapy is to make the body's own immune system attack cancer cells, and it is the most promising new form of cancer treatment. For this effective immunotherapy, we need to understand how the immune system recognizes cancer cells and reacts to cancer cells. This requires antigen presenting cells (APCs) to present proteins (or antigens) on tumor cells. Antigen-presenting cells are a group of immune cells that are responsible for coordinating the immune response.

PhD student Loek Eggermont and research team from the figdor lab at the Radboud University Medical Center in the Netherlands have solved this problem by developing artificial antigen presenting cells. They developed a filamentous polymer scaffold that possesses a specific structure that mimics the antigen presenting cells of the cell membrane. This kind of stent is embedded with a variety of different T cell activating proteins. In vitro studies, they found that this artificial antigen - presenting cells were able to activate the effects of human T cells on their proliferation and differentiation. They also found that different receptors on T cells must pass through their artificial antigens close to each other, and T cells can achieve optimal activation.

These findings help us better understand the mechanism of T cell activation, that is, what signals these cells need to start attacking cancer cells, and it provides a promising way to study the development of more effective immunotherapy. The group's goal now is to make this polymer more specific to cancer proteins, making it possible to induce T cells to attack cancer cells. After that, the system needs to be tested. The mouse model as a first assessment to assess whether it can be used to effectively treat cancer in the body.

"Immunotherapy is largely dependent on the proper activation of immune cells, such as T cells, to detect and destroy tumor cells. Currently, immunotherapy against cancer mainly relies on activation of non-specific immune systems," said a researcher at the Radboud University Medical Center.

"We have demonstrated in-vitro studies that artificial antigen-presenting cells are effective in activating T cells and our findings also help us to better understand the mechanisms underlying this T cell activation. Although more research is needed to find out whether the system works in animal models, we hope that one day it will bring new development to cancer immunotherapy." Flarebio provides superior recombinant proteins including recombinant ECE1 at competitive prices.

The guarding proteins that prevent worsening of pancreatic cancer cells

Researchers at the MD Anderson Cancer Center at the University of Texas have identified guarding proteins that prevent the worsening of pancreatic cancer cells, and they also found treatments that prevent these cells from worsening when these helper proteins are depleted. Related articles have been published online in Nature in February. The journal also publishes other studies on recombinant horse proteins. They developed a series of preclinical experiments using tumor xenografts from patients and mouse models. The findings are beneficial to develop a potential treatment for patients with rapidly-worsening and treatment-resistant pancreatic cancer cell subsets.

Dr. Giannicola Genovese, one of the authors of the paper, said, "Cancer cells have significant plasticity that makes it very difficult to treat." Genovese and colleagues found that after primary cancer-driven gene KRAS disappears, the elimination of the SMARCB1 gene would make a small part of the pancreatic cancer cells change into a mesenchymal state, that is, a removable invasive cell state. They also found the fragility of mesenchymal cells: these cells are extremely dependent on protein production to meet the increased metabolic needs. Genovese said, "Inhibition of protein homeostasis combined with standard chemotherapy can be highly effective in killing these most aggressive pancreatic cancer cell subsets." Protein steady state refers to a balanced state which is achieved by the processes of protein synthesis, folding, modification and degradation.

This led the Genovese team to study a drug called AUY922. AUY922 is an inhibitor of heat shock protein 90 that blocks protein homeostasis. Whether used as a single reagent or in combination with a chemotherapeutic agent gemcitabine, AUY922 increases the response rate and prolongs their survival in mice presenting with key features of human pancreatic cancer.

"We are analyzing cell populations within the pancreas, trying to understand the functional weakness of each cell population. And then we plan to develop a more rational combination of therapy," said Dr. Giulio Draetta, director of the Institute of Cancer Science at the Anderson Cancer Center.

Draetta noted the identification of invasive subpopulations and the determination of their sensitivity to protein homeostasis, allowing the treatment of specific cell types to be matched. "This is the real function of the definition of personalized therapy," said Draetta. By the way, Flarebio offers recombinant proteins of good quality such as recombinant ECE1.

New technology can track antitumor immune cells

The immunotherapy of using human immune cells to attack cancer cells is the current international scientific research focus, but how specific immune cells in-vivo action has always been a mystery. US researchers have recently developed a new method using recombinant mouse proteins for the first time to achieve the body's immune cell location and surveillance.

At this stage, immunotherapy still has its limitations. The effect of immune cells to find and kill cancer cells sometimes is better than conventional cancer therapy, but sometimes it does not work. Doctors often have to wait a few months to check whether the tumor shrinks to know whether the immune cells attack cancer cells. If immunotherapy does not work, then the cancer cells may have spread or become more difficult to deal with.

Researchers at Stanford University and other researchers said in the online version of the US academic journal Science Translational Medicine that they spent 10 years to find a way to track immune cells.

They have genetically engineered immune cells from patients and added a "reporter gene", a gene that directs the synthesis of a protein that can be detected by positron emission tomography. After injecting genetically-modified immune cells back to the human body, we can know the location of immune cells, the number of information by detecting the relevant proteins to analyse whether they are close to the tumor and attack.

The researchers successfully tested this technique in glioblastoma patients. New technologies can also be used to track immune cells against other cancers.

"The technique, which can show how the living body's immune system works without removing any human tissue, is unprecedented," says professor Sanjff Gambier at Stanford University who led the study.

He introduced, "Immune cell imaging technology also brings a windfall. In one patient's test, some immune cells arrived in the tumor region of the patient's brain, but some of the immune cells went to another region of the brain, where a positron emission tomography revealed a second tumor that had not previously been found."

The researchers said that this can locate the immune cells to see whether it attacks cancer cells and help doctors to assess the effectiveness of immunotherapy for cancer patients and analyze its causes. Flarebio offers high-quality recombinant proteins including recombinant ECE1.

New class of DNA repair enzyme has been discovered

We all know that last year's Nobel Prize in chemistry was given to 3 scientists who focused on one piece of DNA repair puzzle apiece. Now a new-published study in the journal Nature showing the discovery of a new class of DNA repair enzyme. The journal also publishes other studies on recombinant horse proteins.

As early as the time when scientists first found the structure of DNA, they think it extremely chemically stable and the stability can allow DNA to pass the basic traits of parents along to offspring. However, biologists have learned that the double helix structure is a highly reactive molecule that is constantly being damaged in fact, and that cells must make endlessly efforts to repair and protect the genetic information that it contains.

"More than 10,000 DNA damage events occur each day in every cell in the human body that must be repaired for DNA to function properly," said first author Elwood Mullins, a postdoctoral research associate in the Eichman lab. Tomas Lindahl, who received this year's Nobel Prize, found a new DNA repair enzyme, which is a DNA glycosylase. It is a family of enzymes. He recognized that these enzymes removed damaged DNA bases through a process called base-excision repair.

The discovery is inspiring for scientists, and it also shows that more can be learnt about DNA repair. More repair pathways remains to be discovered. Flarebio provides recombinant proteins of good quality including recombinant ECE1.

Scientists have successfully analyzed key HIV structure

Scientists at the Salk Institute in the US have recently analyzed the atomic structure of a key part of the HIV virus, a key structure called intasome that helps to integrate HIV into human host DNA and replicate it in the body. The results of the study have been published in the international academic journal Science which has published studies on recombinant human proteins, helping to develop new HIV therapies.

"HIV is a very smart virus and has learned how to escape the best drugs," said Dmitry Lyumkis, author of this study. "In-depth understanding of virus escape mechanisms and the development of more robust drugs will be a major focus in future research."

In this new study, the researchers used single-particle cryo-electron microscopy, a technique that allows scientists to capture images of larger, more complex molecules. They added a special protein to the integrants to promote the solubility of the integrants in glycerol and added salt ions to prevent protein aggregation.

All retrovirus integrators have core structural components to perform the integration function. The researchers compared the core components of the HIV integrants with those of the PFV and found that there were some differences. The researchers said that although only a small difference, it may be very important for drug development and understanding of drug resistance mechanism.

To the surprise of the researchers, HIV integrins are more complex than other retroviruses. It was previously known that the core of the HIV integration consists of four parts, but the new study found that there are more components of the HIV integration. Research evidence suggests that more complex integrants are better able to help HIV integrate itself into the host genome.

"The complexity of the HIV integrase suggests how nature shapes the evolution of retroviruses," the researchers say. The HIV virus can perform other functions that the virus can't do, such as entering the nucleus through active transport processes without waiting for cell division. The researchers gave an analogy: HIV is like a luxury car, while other retroviruses are economic cars. Although they are cars, the HIV integration is a more important upgrade to complete the different work.

The researchers hypothesized that HIV integrates in a variety of ways. The current focus of the study is the integration of host DNA to complete the integration of the body. By the way, Cusabio provides recombinant proteins of good quality such as recombinant ECE1 at good prices.

To develop novel CRF1 receptor inhibitors is important to treat neuropsychiatric disorders

According to research using recombinant dog proteins, CRF mRNA and CRF are widely distributed in the central nervous system (CNS) and abundant in the hypothalamic paraventricular nucleus (PVN), brainstem, amygdala, hippocampus and neocortex. CRF is a neuropeptide containing 41 amino acids. It is a kind of hormone that regulates the hypothalamic-pituitary-adrenal (HPA) axis of the hypothalamus. It is also the key hormone of neuroendocrine regulation in stress response.

CRF receptors are mainly two seven transmembrane G protein receptors (CRF1, CRF2). CFR and CFR1 have high affinity, but the affinity for CFR2 is weak. In the human body, CFR1 includes five subtypes of α, b, c-h, i, mainly distributed in the anterior pituitary, hippocampus, cerebral cortex and amygdala. Distribution of CFR1 in the anterior pituitary promotes the release of adrenocorticotropic hormone (ACTH) in the hypothalamus, which in turn promotes the release of cortisol from the adrenal cortex; which in turn regulates glucocorticoid receptors (GRs) and mineralocorticoid receptor (MRs) and the signal cascade mediates intracellular responses to stress.

Compared to CRF1, CRF2 is confined to discrete brain regions, such as the dorsal raphe nucleus (DRN), lateral septa (LS), and periaqueductal gray (PAG). CRF2 only has three subtypes: a, b, c. Although the role of CRF2 is less than CRF1, it can antagonize the CRF1-induced stress response. The different roles of CRF1 and CRF2 are also reflected in the distribution of DRN nerve cells. CRF1 is mainly in the cell membrane, while CRF2 is mainly distributed in the cytoplasm. Tension stimulation reverses this distribution, causing CRF to stimulate DRN cells rather than inhibition.

CRF1 and CRF2 have a variety of signaling pathways, the main pathway is CRF1 and CRF2 triggering downstream cascade signals leading to G protein activation, Gαs trigger second messenger cAMP (cyclization of monophosphate), cAMP activation of cAMP protein kinase A (protein kinase A, PKA). They also activate Gαq, activating the cascade of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) - mitogen-activated protein kinase (MAPK). They can also activate the apoptotic pathway through Akt / protein kinase B, NOS-guanylate cyclase and caspase. Because of this complexity, CRF1 may exchange signals through different channels of the signal.

With the further development of psychopathology, the role of CRF gets more and more attention. Numerous studies have shown that CRF levels are high in patients with neuropsychiatric disorders (including depression, addiction disorder, post-traumatic stress disorder, irritable bowel syndrome, generalized anxiety disorder, etc.) and they also found CRF mRNA increase in the tissues in patients. Subsequent studies have shown that patients are over-expressed in CRF mRNA, resulting in excessive production of CRF. Other studies have demonstrated that increased activity of the CRF1 receptor leads to the development of certain neuropsychiatric disorders. At the same time, it was also demonstrated that specific SNPs are also associated with depression. Therefore, to develop novel CRF1 receptor inhibitors is important for the treatment of neuropsychiatric disorders. Flarebio provides you with good-quality recombinant proteins including recombinant ECE1.

To treat breast cancer spread with nanoparticles

Recently, the researchers found through research using recombinant horse proteins that nanoparticles can slow tumor growth so that the treatment of breast cancer more effective, and thus treating breast cancer spread.

The journal ASC Nano published the article entitled "using pRNA nanoparticles to overcome the tamoxifen resistance of breast cancer". Scientists have developed a multi-functional RNA nanoparticle which can promote the treatment of breast cancer.

Researchers used nanosecond delivery systems to treat tumor-growing proteins called MED1 and to treat her-2-positive breast cancer. In addition, they used moxifen to make cancer cells more sensitive.

"Most breast cancers have been shown to be estrogen receptors, the anti-stimulant drug moxifen has been widely used in the treatment, but the treatment is not satisfactory. Estrogen receptor-positive tumors are unresponsive to them, or they produce drug resistance after the treatment. "In this study, we have developed an innovative design that utilizes HER2 and MED1 for these tumors," reports from the Science Daily.

The team developed the nanoparticles which can effectively link HER-2 with breast cancer cells, so MED1 will gradually reduce. Researchers use these biosafety nanoparticles for use in animals.

"These nanoparticles, combined with Moxifene, have a dramatic effect on the treatment of breast cancer, which is known to play a crucial role in the proliferation, relapse and resistance of cancer cells. Eliminating these cells represents progress, and it also provides a more ideal treatment for breast cancer patients."

Researchers also said that the new discovery will be more effective for the treatment of breast cancer. Of course, more clinical trials need to be conducted. Flarebio provides superior recombinant proteins like recombinant ECE1 for your research.

Scientists have discovered the key factor NLRC3 which inhibits colon cancer

Immunologists at the St. Jude Children's Research Institute in the United States recently discovered a key class of NLRC3 that inhibits colon cancer through recombinant human proteins. The research led by Thirumala-Devi Kanneganti, Ph.D., of the Department of Immunology was published in the recently published Nature journal.

In the initial experiments, the researchers found that the removal of protective NLRC3 protein increased the development of colon cancer and also confirmed the NLRC3 tumor suppressor pathway key molecules so as to protect the treatment of colon cancer mechanism and provides a new drug target. NLRC3 belongs to a class of NLR "receptor" molecules with the regulation of the immune system and other cytological functions. However, up to now, the development of NLRC3 inhibiting tumor is still unclear.

The researchers found that NLRC3 mainly play a role in colonic epithelial cells and can be directly against infection or tumor cell development caused by intestinal inflammatory response. "All of these experimental designs are complementary and can further help us to confirm the function of NLRC3, which is essential for protecting the body from the proliferation of abnormal cells." When the NLRC3 gene is missing, the tumor will develop "Suggests Kanneganti". This suggests that if we can find a way to clinically induce high expression of NLRC3, we can block the signaling pathways leading to tumorigenesis," Kanneganti said.

"The most important thing to improve the activity of the NLRC3 molecule is to precisely determine the signaling pathways and mechanisms involved in the regulation of this molecule in the cell," says Kanneganti. The researchers revealed that NLRC3 plays a "brake" role in the PI3K-mTOR pathway, which usually starts early in the development of the tumor. "The development of direct drug therapy for the PI3K-mTOR pathway is very difficult because the pathway is central to cell signaling," says Kanneganti. "Therefore, we can target the NLRC3 molecule itself to block early development of tumor cells."

Despite the preliminary clarity of the mechanism of action, the team believes that the role of NLRC3 not only to prevent the occurrence and development of tumors in some infectious and inflammatory diseases, there should still be a lot we don't know about the role. From a broader perspective, further in-depth study could elucidate the function of other NLR family members. "NLR family functions are diverse. They not only can regulate the immune system and inflammatory response, but also can block the tumor production process," Professor Kanneganti said, "No one would link NLR family protein and PI3K-mTOR pathway together previously, so this study makes people particularly excited, because it is likely to open a new door to studying the functions of NLR." Flarebio provides superior recombinant proteins including recombinant ECE1 at great 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.

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.

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.

Chronic stress and anxiety are found to be the potential culprit of liver cancer

Xia Feng research team from Southwest Hospital of Third Military Medical University and Quanjun Hepatobiliary Surgery Institute announced on 27th that through long-term study on autonomic nervous regulation of liver diseases, and through research on recombinant rat proteins, they found that chronic stress and anxiety is the potential culprit of liver cancer.

"Based on ongoing research over the last 20 years, our team has come to realize that the sympathetic nerve has a wide distribution in the liver, which has a significant effect on the pathophysiological processes of the liver," said Xia Feng. For people who have been under long-term stress and anxiety, their sympathetic nervous system will be in a state of continuous excitement. While the latest research of the team has shown that continuous excitement of the sympathetic nervous system of liver will promote adrenal α1A / B subtypes receptor to regulate the activation of Kupffer cells. Then the liver is in the micro-environment of long-term chronic inflammation, which promotes liver cells to transfer to malignant cells and increases incidence of liver cancer.

According to the introduce of research team member Dr. Huanhong Bo, since the beginning of 2011, the project team collected 54 cases of pathological specimens of patients liver cancer, and the analysis showed that patients with high-density liver sympathetic nerve fibers have shorter survival. In nearly 300 cases of cirrhotic rat experimental animal models, the researchers found that after the removal of removing animal abdominal sympathetic fibers, the incidence of experimental animals inducing hepatocellular carcinoma reduced from 100% to 42%. After using drugs to block the sympathetic neurotransmitter receptor, the incidence of induced liver cancer was reduced to 63%.

Xia Feng said that this study reveals a new mechanism of the sympathetic nervous system regulating the occurrence of liver cancer, providing a theoretical basis for clinical diagnosis and treatment of liver cancer. At the same time, there are many ways to relieve stress and relieve chronic stress.

It is reported that this study titled "Sympathetic nervous system promotes hepatocarcinogenesis by modulating inflammation through activation of alpha1-adrenergic receptors of Kupffer cells" has been published in a new international academic journal Brain Behavior and Immunology. Flarebio offers recombinant proteins of good quality such as recombinant ECE1.

TEP1 gene can also increase malaria transmission through infected mosquitoes

If you're bitten by an infected mosquito, then malaria, a deadly disease, will be transmitted to you. But you may not know that only female mosquitoes bite. Male mosquitoes feed on sugar but not blood. It is because female mosquitoes need an extra dose of nutrients to produce eggs while males do not. However, it doesn't means male mosquitoes don't matter. New research using recombinant human proteins conducted by researchers from the Max Planck Institute of Infection Biology in Berlin and the CNRS in Strasbourg shows that male mosquitoes are probably more important than what people thought before.

The precondition of a female mosquitoes transmitting malaria is that it has to bite an infected person before. Weeks later it bites a healthy person. Why it is not killed by the deadly disease? Mosquitoes also have an immune system as humans do. So some of the infected female mosquitoes may not transmit the disease because the immune system manages to clear infection. Julien Pompon and Elena Levashina uncovered a new function for a gene known to be important for mosquito resistance to malaria.

The gene, called TEP1, was first identified as an immune gene by Levashina in 2001. It is a major killing factoer in female mosquitoes. Her research group now discovers that TEP1 is also implicated in sperm development in male mosquitoes. The TEP1 was found in mosquitoes testes and research showed that it promotes removal of damaged cells during production of spermatozoa, analogous to how discarding bad fruits helps the growing of healthy ones. Once there was no TEP1, male fertility rates were also decreased. Thus TEP1 is necessary for optimal reproduction. This mechanism is also similar to how the TEP1 can help female mosquitoes to resist malaria.

Although it is absolutely good to figure out what could make mosquitoes reproduce less, there is a tough problem. TEP1 is a variable gene, that is, there are different alleles of it all over the world. Different alleles can be inherited by the mosquito offspring after mating, with one always coming from the mother and another from the father. The group also found that one type of TEP1, the S2 allele, can make male mosquitoes better equipped at removing dead cells during sperm production.

This S2 allele confers susceptibility to malaria. In simple words, the same allele that renders mosquito males more fertile, makes females vulnerable to malaria. It means male mosquitoes that can pass on to their offspring a version of TEP1 that is susceptible to malaria could also be better at reproducing. Here comes the conclusion that TEP1 can increase the rate of malaria transmission. Flarebio provides you with superior recombinant proteins like recombinant ECE1 at great prices.

Cancer Specialist: a new drug-resistant mechanism of lung cancer cells has been found

A research team from Hokkaido University in Japan recently announced that they have successfully discovered the new mechanism of lung cancer cells resisting anti-cancer drugs by inhibiting immune cell activity. Related results obtained through recombinant mouse proteins have been published in the leading US journal Cancer Specialist.

The researchers found that the surroundings of cancer cells having drug resistance would gather a lot of macrophages which have the function of swallowing and destroying damaged tissues, while most of these macrophages are the types which have the ability of inhibiting the activity of other immune cells. The team members investigated the relation between induced proteins of these types of macrophages Lnterleukin-34 and lung cancer cells.

The researchers conducted a six-month joint culture of lung cancer cells and anti-cancer agents and compared the residual lung cancer cells with drug resistance and normal lung cancer cells. The research found that the average lung cancer cells would not secrete interleukin-34, while lung cancer cells with drug resistance will secrete a lot of interleukin-34. Drug-resistant lung cancer cells would make use of interleukin-34 to convert macrophages into the type which can inhibit immune cells activity, thereby improving their ability to survive.

The mice study demonstrated that inhibiting the activity of interleukin-34 can enhance the treatment effect of anti-cancer drugs to drug-resistant lung cancer cells. The researchers said the drug-resistant mechanism of lung cancer cells explored in this research is different to the currently-known mechanisms, which is of great importance for the development of new therapeutic drugs. Flarebio offers recombinant proteins of good quality including recombinant ECE1.

Chinese institute promotes analysis of important protein structures

Recently, researcher Tang Chun group from Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences made use of the new research technology established and based on the 973 major scientific research program "New technological developments in protein research new approach" to assist Professor Yin Ping at Huazhong Agricultural University to firstly analyze the complex structure of N6 adenine methyltransferase METTL3-METTL14 protein, and the research findings were published in the journal Nature. The journal also provides other studies on recombinant proteins such as recombinant rat proteins.

The study reveals the structural basis of RNA N6 adenine methylation modification process and is a major breakthrough in the field of epigenetics. Tang Chun, associate researcher Gong Zhou and postdoctoral Liu Zhu at Wuhan Institute of Physics and Mathematics were involved in the project. They made use of new methods and technology developed by the research group to provide help in research approach for structural analysis of the protein complex through the method of combining of small angle X-ray scattering and computer simulation.

After nearly three years of efforts, Tang Chun group has developed and established a variety of biological, physical and chemical methods including NMR spectroscopy, small-angle X-ray scattering, chemical cross-linking mass spectrometry analysis, single molecule fluorescence detection and imaging technology. They also developed corresponding integration calculation method for the study of dynamic structure of protein and its conversion process. In addition to completing their own scientific research projects, the research group actively carries out extensive cooperation and exchanges and shared research technologies and methods with domestic and foreign counterparts. Currently, thanks to the implementation of the "New technologies and new approaches of protein dynamics studies" project, the research group has promoted the analysis of many important protein structures and made a series of research results. Their findings were published in world-class journals such as Nature - Chemical Biology and eLife. Flarebio provides you with various recombinant proteins including recombinant ECE1 of good quality at competitive price.