New breakthrough has been made in the study of breast cancer targeted treatment

Dr. Xu Lingzhi and his research team from the Second Affiliated Hospital of Medical University in Dalian have made new achievements in the field of breast cancer stem cell properties and targeted therapy. The achievements describes the key regulating effect of p62 / SQSTM1-let-7a / b-MYC signaling pathway on breast cancer stem cell properties for the first time and indicates that signaling hub protein p62 / SQSTM1 can be an effective target for intervention, providing new thoughts for overcoming the recurrence, metastasis and drug resistance of breast cancer. Related research papers are recently published online in the journal Cancer Gene, which also publishes some other studies on recombinant human proteins.

Currently, the clinical treatment of breast cancer has been improved greatly, but the phenomenon of recurrence and drug resistance is becoming more serious. More and more evidence suggests that tumor stem cells are highly correlated with drug resistance, relapse and metastasis during tumor treatment. However, because of the dynamic evolution and high-degree heterogeneity of tumor stem cells, therapies aimed at cancer stem cells still lacks for effective targets and intervention mechanisms.

As a "signal hub" within the cell, p62 / SQSTM1 protein combines with a variety of signaling molecules through its own series of functional domains to be involved in the regulation of various signaling pathways. In the study, researchers took breast cancer as an example. By in-vitro and in-vivo animal experiments of cell lines, the researchers reveal the signaling protein p62 / SQSTM1 highly express in cancer stem cell enriched population for the first time, and it plays positive regulation role to "dry” character of tumor stem cells. Intervention of the expression of the gene can significantly reduce the "dry" character of tumor stem cells. The research team also found that the signaling protein p62 / SQSTM1 can promote mRNA stability after oncogene MYC transcription by reducing the expression of a small RNA-let-7a / b, thus mediating "dry" phenotype of tumor stem cells. Subsequent analysis of clinical samples further validated that the high expression of signaling protein p62 / SQSTM1 was negatively correlated with PFS and OS in breast cancer patients. Flarebio provides high-quality recombinant proteins such as recombinant CDH4 at good prices.

Get to learn more about the role of PARP in cardiovascular disease

Poly ADP-ribose polymerase (PARP) is a protein which is widely concerned in the field of cancer treatment in recent years, for it plays an important role in the DNA repair process. PARP activity lies in that it conducts ADP-ribosylation to its substrate proteins through NAD +. When DNA shows breakage, PARP is activated and then makes histone ADP at break sites ribosylated, prompting histone seperates itself from DNA molecule, thereby conducting combination before repairing proteins. The findings were obtained through recombinant rat proteins. On the other hand, because the rate of rapidly DNA breaks of cancer cells which separate rapidly is quite frequent, once PARP is inhibited, DNA damage can accumulate quickly in the cancer cells, ultimately leading to cell death.

However, the role of PARP is not limited to DNA repair, and its medicinal value is also not limited to this. Recently, scientists from the US Southwestern Medical Center have found a wide range of functions in the PARP gene transcriptional regulation and RNA processing, opening up a new direction for cancer therapy development. Their results were published in the recent issues of Science.

"This discovery changes our understanding of the function of PARP, which may open a new field of drug development," corresponding author of the article Professor W. Lee Kraus said.

To systematically analyze the intracellular function site of PARP, the researchers transformed PARP so that it can conduct ADP-ribosylation NAD + substrate proteins which are modified by acetylene group, thus the introduction of the ADP ethynyl cycloaddition reaction may occur with fluorescently labeled molecule with an azide group, thus marking and identifying a number of PARP in cells in vitro substrates, including a variety of proteins as well as sites on the chromosome.

The negative transcription elongation factor (NELF) attracted special attention of researchers. NELF is involved in the pause process of RNA transcription, and this is to ensure that there is enough intracellular ribonucleotide used for the mechanisms of transcription. Under normal circumstances, PARP will conduct ADP- ribosylation to NELF, thus sending the signal of sufficient supply to NELF so that transcription can proceed.

"We found that the modifications of PARP to NELF can alter open or closed state of the gene in breast cancer cells, thus affecting the biological state of a cell fundamentally," Professor W. Lee Kraus said, "This is a newly-discovered link." Flarebio offers recombinant proteins of good quality including http://www.cusabio.com/Transmembrane-Protein/Recombinant-Human-Integrin-beta-2ITGB2-11153649.html" title="http://www.cusabio.com/Transmembrane-Protein/Recombinant-Human-Integrin-beta-2ITGB2-11153649.html"recombinant ITGB2 at competitive prices.

New potential tool of tagging innocuous protein

As we know that proteins and peptides of various sizes and shapes have been used since the early 80s to tag proteins with many different purposes, ranging from affinity purification to fluorescence-based microscopic detection in whole organisms. However, tagging strategies used nowadays run the risk that the native function of the protein may be abolished or compromised by interactions with the tag.

A study using recombinant proteins like recombinant horse proteins published yesterday at Nature Methods proposes the use of two plant protein epitopes, named inntags, as the most innocuous and stable tagging tools in the study of physical and functional interactions of proteins.

The study is leaded by the Molecular Biology Institute of Barcelona and the Joint Programme for Computational Biology of the Institute for Research in Biomedicine (IRB Barcelona) and the Barcelona Supercomputing Center, and University of Barcelona. It has analyzed the available list of polypeptides with known 3D structure to identify among them the most suitable for tagging purposes. Researches have selected the smallest protein domains that still display strong structural determinants to act as antigens, do not generate solubility issues, do not compromise cell fitness and cause no detectable functional and localization effects when fused to other target proteins.

A large series of bioinformatics tools were first used to scan through the entire planet proteome to select those proteins which could have good tagging properties. After manual curation of the in silico results 12 tag candidates were tested in vivo, finding excellent or outstanding properties for all of them. Inntags maintain their integrity, stability, solubility in cell extracts, diffusional mobility and do not cause important functional perturbations that commonly used tags -such as MYC, FLAG or HA- do cause. Moreover, the tests have shown the applicability of Allergen Phl p2 and Heiven Isoform 2 in immunofluorescence and immunoprecipitation analysis of a series of proteins in mouse fibroblasts and hippocampal neurons.

Compared with commonly used tags, inntags are clearly more innocuous. They may be the tools of choice to perform proteome-wide interactome studies, in situ analysis of proteins at the single-molecule level or when the target protein does not offer an obvious functional assay. The tools are believed to open new possibilities for researchers in cellular biology. Flarebio provides superior recombinant proteins such as recombinant APP at competitive 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.

NRG1 protein can help to effectively treat Alzheimer's disease

According to news from RIA Novosti on August 25th, US neuroscientists made use of recombinant human proteins and found an upgraded brain protein - neuregulin 1 (NRG1) and this protein can effectively help to treat Alzheimer's disease.

It is generally throught that Alzheimer's disease is due to too much amyloid pathogenic substance called β-amyloid protein depositing inside neuron. Such β-amyloid protein is formed from β-amyloid precursor protein (APP) proteolysis. It is involved in repairing damaged proteins and can be combined with protein molecules. β-amyloid protein can lead to the emergence of amyloid plaques and death of nerve cells.

While scientists from the United States Institute of Biology Khajuraho Cambiasso Turk have recently discovered a protein having a clear function - neuregulin-1. The protein can’t only clear the protein plaques in the brain but also can slow down the formation of β - amyloid plaques.

Scientists conducted experients with mice suffering from Alzheimer's disease. They put a special virus containing neuregulin-1 proteins in brain of the lab mice. The purpose is to make the neuregulin-1 genes grow in mice. During the process of experiment, the scientists made the mice to look for exit, and then they observed whether neuregulin-1 proteins would improve the memory capacity of mice and make the protein plaques in their neurons decrease. Experiments show that the neuregulin-1 protein does improve the memory capacity of mice and remove β- amyloid protein plaques.

Currently, scientists still don't know the specific reasons for this phenomenon. But they believe that neuregulin-1 protein can promote to form another peptide - enkephalinase enzyme which can solubilize protein agglomerate. However, whether the fact is true remains to be verified through the results of recent experiments.

Besides, scientists also said that the main advantages of neuregulin protein is that it can move freely through the barrier between the brain and the rest of the body, thus it can be flexibly used to treat Alzheimer's disease. Flarebio offers recombinant proteins of good quality such as recombinant EXT2.

The problem of plants facing with high salt can be saved by some newly-found proteins

Previous studies show that high salt in soil dramatically stresses plant biology and reduces the growth and yield of crops. A study led by professor Staffan Persson who is interested in producing recombinant proteins like recombinant rat proteins, from University of Melbourne, Australia, formerly at the Max Planck Institute of Molecular Plant Physiology, found specific proteins that allow plants to grow better under salt stress, and may help breed future generations of more salt-tolerant crop plants.

Humans can move away from the salty snacks or drink more water, but if a plant is stuck in high salt (or saline) soils, it must use other tactics to cope. More and more of the world' crops are facing salt stress with high salt in soils (also known as salinity) affecting 20% of the total, and 33% of irrigated, agricultural lands worldwide. We need to increase production of food by 70% to feed an additional 2.3 billion people by 2050. Salinity is a major limiting factor for this goal as more than 50% of the arable land may be salt afflicted by the year 2050. Thus finding genes and mechanisms that can improve plant growth under such conditions is of utmost urgency.

"Plants need to make bigger cells and more of them if they want to grow and develop, " said Prof Persson, which is good at producing recombinant proteins like recombinant horse proteins.

"Unlike animal cells, plant cells are surrounded by a cellular exoskeleton, called cell walls which direct plant growth and protect the plant against diseases. Importantly, most of the plants biomass is made up of the cell wall with cellulose being the major component. Hence, plant growth largely depends on the ability of plants to produce cell walls and cellulose, also under stress conditions, and it is therefore no surprise that research on cell wall biosynthesis is of high priority."

The present study shows that an previously unknown family of proteins supports the cellulose synthase machinery under salt stress conditions, and was named "Companions of Cellulose synthase (CC). These CC proteins are part of the cellulose synthase complex during cellulose synthesis. The researchers found that the CC gene activity was increased when plants were exposed to high salt concentrations.

"In an additional step, we made fluorescent versions of the CC proteins and observed, with the help of a special microscope, where and how they function. It was quite a surprise to see that they were able to maintain the organization of microtubules under salt stress. This function helped the plants to maintain cellulose synthesis during the stress", said Dr. Anne Endler, co-first author of this study.

The research group proved that the plants lacking the CC activity were unable to maintain their microtubules intact. The loss in microtubule function led to a failure in maintaining cellulose synthesis, which explained the reduction in plant growth on salt.

The results of the study provide a mechanism for how the CC proteins aid plant biomass production under salt stress and help plants to grow on salt. The team has identified a protein family that helps plants to grow on salt, and outlined a mechanism for how these proteins aid the plants to produce their biomass under salt stress conditions. The study was published the day before yesterday in the journal Cell. Flarebio provides good-quality recombinant proteins like recombinant CD44 at competitive prices.

A kind of blood thinner can decrease risk of bleeding

In an industry-university cooperation, researchers developed an antibody that can prevent the formation of blood clots but does not trigger bleeding. Bleeding is a serious risk associated with a currently-used blood thinner.

The study was carried out on a variety of animal models using recombinant proteins such as recombinant dog proteins. In order to prepare the safe drug use in human body in the future, they also developed a second antibody which can quickly reverse the effects of the former drug, thus providing additional security measures to guard. Blood clots can cause heart attack, stroke and other cardiovascular diseases. Patients suffering from these diseases often use drugs to prevent blood clots, but it will bring a high risk of uncontrolled bleeding. Coagulation Factor XIa (FXIa) is the protein which plays a key role in the formation of blood clots. It has become a major drug target, but to achieve specifical inhibition of FXIa remains difficult.

Therefore, Tovo David and colleagues designed an antibody which is capable of binding specifically to FXIa and block activity of FXIa enzyme. The antibody can prevent blood clotting in the human body as well as mice and rabbits. The drug seems to be safe in the body of monkeys, because even giving dose which is much higher than required dose to prevent the formation of blood clots in monkeys, the monkeys didn't show signs of spontaneous bleeding. Although there is no increase in bleeding was found in these animal studies, FXI deficiency may be associated with bleeding in human body. Thus, the researchers developed a second antibody which can act as antidote that can rapidly reverse the activity of anti-FXIa antibody.

Through further research, reversible FXIa specific antibodies may provide a novel and potentially safer anticoagulants. Flarebio offers recombinant proteins of good quality such as recombinant Stim2.

To use gene therapy to replace retGC1 to restore visual function

Not so long ago there was a research about using gene therapy to replace retGC1 to restore visual function. In the research with recombinant proteins, mice lacking the protein retGC1, which is deficient in humans suffering Leber congenital amaurosis-1 (LCA1), a disorder that causes severe visual impairment beginning in infancy, received gene therapy to replace retGC1 and showed fully restored visual function that persisted for at least 6 months. The success would strongly support clinical testing of a gene therapy targeted to the retinas of LCA1 patients as the researchers concluded.

Sanford Boye, Shannon Boye, and coauthors from University of Florida College of Medicine, Gainesville, University of Oklahoma College of Medicine, Oklahoma City, and Salus University, Elkins Park, PA, are the authors of the article. They emphasize the need for a treatment strategy targeting the loss of cone function that occurs in the eyes of patients with LCA1. They describe a gene replacement approach that uses an adeno-associated viral (AAV) vector to deliver the gene encoding the retGC1 protein to the cone-rich central retina in an all-cone mouse model deficient in retGC1. They report their results conclusions in the article.

"This study shows the tremendous potential of recombinant (rAAV) gene therapy for the effective treatment of genetic causes of vision loss," says Editor-in-Chief Terence R. Flotte, MD, Celia and Isaac Haidak Professor of Medical Education and Dean, Provost, and Executive Deputy Chancellor, University of Massachusetts Medical School, Worcester, MA.

This article about the Gene therapy is available free on the Human Gene Therapy website before September 30, 2015. Want to know more? Go and see! Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. It offers recombinant proteins like recombinant KEL at good prices.

SemaA2 and PlexA2 protein play important role in the process of retina function

How do our eyes interpret the world around us to find moving objects?

Scientists who study eyes of mammals don't know too much about the molecular clues which are used to probe neural circuits of movements. But through use of recombinant human proteins, they know that SACs' astrocytes located in the photosensitive layer (or retina) of eyes is within a related to this.

SACs can detect movement by making reaction to bright and dark light. They will then communicate with other nerve cells despite that their communication modes in SAC cells are different in the condition of "light" and "dark". How do the same SAC cell types obtain these opposite functions is still a mystery.

Now, scientists from Johns Hopkins University School of Medicine are focusing more on understanding how neural circuits in the eyes interpret the light pattern to permit detection of movement. They focus on a pair of retina proteins called SemaA2 and PlexA2.

In this study, the scientists designed the retina of mice to make it lack for one or two such proteins and observed how this would affect the function of SAC cells. Each time, SAC would change cell reactivity. Mouse retina containing mutant SACs showed poor performance in reactive test. It is vital that cutting expression of SemaA2 can help to create two different SAC cell groups (light and dark) which have opposite structures and functions.

This finding suggests that SemaA2 and PlexA2 can collaborate to make mammal retina grow healthily and function well. Flarebio offers recombinant proteins of good quality such as recombinant Cdh8 at competitive prices.

Scientists find the turning point that determines protein fate

The scientists just "resurrected" the ancient ancestor of an important human protein and studied its evolutionary history which has always constantly showing mutations and analyzed a large number of alternative histories. Research shows that only two special mutations occur can ancient proteins evolve into modern glucocorticoid receptor (GR). These two permissive mutations have no effect on protein function, but they are the key base of functional mutations. The researchers screened thousands of evolutionary pathways and found that ancient GR evolved the sensitivity to cortisol in only one way. Related research papers were published in the journal Nature which also published many other studies on recombinant proteins.

Senior author of the paper, Professor Joe Thornton said, "This key protein can exist because there is a turning point in the destiny. Maybe the evolution of many body systems is dependent on the rare events in evolutionary history." He inferred the possible sequence of ancient proteins and synthesized biochemically and introduced them into a living organism to study their function.

Researchers deeply analyzed the structural effects of mutations on ancient proteins and found such rare causes. Such mutations must meet three conditions: it must stabilize specific regions in protein structure; to maintain proper energy balance among functional conformations; and it can be compatible with the original architecture and derived structure. Few mutations can meet such stringent restrictions.

The researchers found that asiding permissive mutations and only introducing functional mutations, ancient GR can't evolve into what it is today. Subsequently, they build millions of gene copies of ancient GR and introduced random mutations into each copy and simulated various possibilities in the evolution. They also produced recombinant rat proteins and designed genetically-engineered yeasts, which only grow when functional GR comes out. The researchers introduced various mutant GR into these yeasts. One any permissive mutations occur, GR function can be restored and allows yeasts to grow. Studies have shown that except two permissive mutations in reality, other mutations all can't restore GR function.

This study helps people further understand the evolution process of protein function. "Being able to directly study variable historical events is very exciting," Thornton said. "If the evolutionary history happens all over again, the results may be completely different. For cellular biochemical systems, unpredictable genetic events also shut down other possibilities when opening an evolution door."

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Pathogenic proteins are not always "bad thing"

In recent years, through research using recombinant horse proteins, some scientists have speculated that aggregation of protein in cells typically plays an active role. Biochemistry Professor Yves Barral ETH Zurich and his research team indicated in 2013 that the memory experiences of yeast cells which takes the form of protein aggregation is related to the unsuccessful experiences related to the attempts of sexual reproduction. These aggregates are not the same with newly-found protein aggregates related to aging. Thus these aggregates can be molecular memory of yeast cells. Even in mice, prion-like aggregates also show a positive correlation with memory. A few months ago, US scientists proved that mice having such aggregates in nerve cells showed a more stable long-term memory.

No matter whether such age-related protein aggregates is originally a fault or a normal function of healthy cells, it is a matter of science for Barral - in which philosophy also plays a role. "Our western society understands aging mainly on the negative, it is a disease that needs to confront the disease," he said. "This idea is reflected in the work of many scientists. The focus of aging research is to find defects in cells." While another view is that the newly-discovered aggregates are the information and memory storages of cells.

"We are still a relatively-small group of scientists who think that protein aggregates are not pathological - they are neither accidental nor defects," Barral said. In contrast, these proteins aggregate because of their normal functions. Diseases like Parkinson's and Alzheimer's diseases only happen when the system becomes unbalanced and too many prion-like proteins aggregate at the wrong sites in cells. Barral continued, "Aging has two sides: you die at the end of life process, which is the negative side; but you die when you are awake. While Alzheimer's disease probably starts well but ends badly."

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Scientists uncover the mystery of animals making orientations

Researcher Xie Chan from Key Laboratory of Membrane Biology of College of Life Sciences at Peking University and his research team found a protein complex through experiments on Drosophila genomes. This protein complex can make orientations in magnetic field and this protein gene is found in a number of animal species. The researchers named it magnetic induction protein (MagR). Related papers were published online in the journal British Nature Materials, which also publishes many other studies about recombinant proteins like recombinant mouse proteins.

In nature, many species of animals have the ability to perceive the Earth's magnetic field. They can sense direction, strength or inclination of magnetic field, and they take the navigation of such information as a clue. Although multiple biochemical models which have already existed before can explained the ability of such animals, scientists are still not clear about the biological mechanism behind it.

By using assumed biological criteria to screen Drosophila genomes, Xie Can and his research team discovered a protein like polymer - magnetic induction protein. This protein will combine with the component of photosensitive Cryptochrome protein (referred to Cry) and spontaneously align the external magnetic field. Through biochemical and biophysical method, the researchers found that Drosophila missing photosensitive Cryptochrome protein don't have the capability of magnetic induction. This indicates that the photosensitive Cryptochrome protein is a necessary condition to make Drosophila produce magnetic sensing capability, but theoretically photosensitive Cryptochrome protein can't form a "compass" role. Therefore, the researchers believe that only the combination of magnetic induction protein and photosensitive Cryptochrome protein makes the animals get awareness of magnetic field.

The researchers found that the magnetic induction protein and photosensitive Cryptochrome protein complex (MagR / Cry) stably exists in pigeons, butterflies, rats, whales and human body. The researchers said that the mechanism of this protein complex sensing magnetic field is unclear. However, discovery of such a protein complex like a compass makes magnetic induction protein have broad application prospects in the aspect of magnetic field regulating biological processes in the future. Flarebio provides you with high-quality recombinant proteins such as recombinant APP at competitive prices.

They are trying to create a protein molecule which can effectively prevent protein allergy

Protein engineer Aaron Chevalier at Seattle forecasts that molecular origami technology will be the future of drug discovery. Tired of producing recombinant proteins such as recombinant dog proteins, he and his team of researchers from University of Washington spent a lot of time to design a complex folded amino acid chains to create molecules which are not found in nature. Their goal: to create a protein molecule and make it bind to pathogenic virus so as to achieving the purpose of preventing virus-infected cells; Or to create a protein molecule which can effectively prevent protein allergy.

It is unclear whether our immune system accepts new foreign protein, because the body may show immune rejection. Moreover, even these proteins show normal reactions on the computer, maybe it fails inside the body due to an unknown reason. In fact, to get these proteins designed to be our medicine cabinet, it will take some time. Baker said, "Like other drugs, before applied to the human body, these proteins must go through clinical trials."

"This process is very complicated - we should not only consider the interaction between proteins but also the problem of side effects as well as the problem of environmental impact on protein function and protein transcription and translation issues and so on." said Zhang Yang, biochemistry Professor at University of Michigan and protein engineering specialist. For the designed proteins, we should not only care about its shape, but also care about the function and stability.

Baker team can use a software program to build a model of the desired protein and indicate the size, shape, chemical properties and working methods of the protein. Meanwhile, Rosetta software can provide a lot of options for testing. At the same time, they can use the Rosetta protein to design and improve the model. This software can identify a mass of amino acid combinations and can find the proteins with desired shape, size and chemical properties. It is more intelligent than producing recombinant proteins like recombinant human proteins.

Once Rosetta completes protein design, scientists will test the protein. Then they will look for required DNA sequence online and implant these DNA sequences into bacteria or yeast to transcripte and translate to get new proteins.

Chevalier designed proteins based on virus antibody, and such proteins can achieve better therapeutic effect by locking the virus in human cells. Meanwhile, Rosetta software will give Chevalier some alternative protein structures to reduce the workload.

Chevalier said, "If considering properties of the antibody, you will find that it can circulate in human body through blood circulation. There is no need to consider frozen state storage transportation when designing, let alone the problems of mass production, solubility and refining concentration." Chevalier hopes he can start from scratch to create proteins possessing these characteristics to make it as a new drug which is low-cost and with stable structure. Flarebio offers high-quality recombinant proteins such as recombinant INSRR.

The trails of preventing deterioration of DLBCL

Recently, a new therapeutic drug is in its clinical Phase II experiments. The drug is mainly for those patients with deterioration of diffuse large B-cell lymphoma (DLBCL), because most of these patients will show tumor metastasis over time. The main target of this drug is histone modifying enzyme, and this target shows obvious effect on some tumor with genetic variation. The design of experiments was mainly done by Sarit Assouline, a blood disease oncologist in Jewish hospital and he is also very interested in producing recombinant proteins like recombinant horse proteins. And the research results have been published in Blood, which is the top journal in Hematology.

Dr. Assouline, associate professor of medical oncology at McGill University said, "DLBCL is a relatively common form in lymphoma and has relatively-high invasiveness. With the deterioration of the disease, there is no effective clinical treatment. The patients have an average life expectancy of 6 months. Our task is to find a new specific target in turn to improve the prognosis of patients, but many clinical trials are just focusing on the patient's response to different treatments. Our aim is to be able to better improve the effectiveness of the treatment on the basis of understanding the mechanism of disease."

Among DLBCL patients, up to 40% of them who receive conventional chemical immunotherapy, stem cell transplantation or several joint treatments still show no effects. New treatment method has a stronger against nature on the basis of deeply explaining molecular structures. Almost all of DLBCL patients contain mutations of histone modifying enzyme gene, so histone acetyl transferase inhibitors have a significant effect on the level of improving the treatment of patients.

In the experiment, subjects went through complex genetic analysis and strict distinction. 28% of patients respond well to the above treatment, and the expression of MEF2B gene was closely related to the curative effect of patients. By analysis of collected biopsy and blood samples, the study revealed that this drug can affect a series of proteins in the body of these patients. If we can take advantage of the latest diagnostic technology to assist, the effect will be better. Flarebio provides superior recombinant proteins like recombinant NRG3 at competitive prices.

New pathway of cancer cell metastasis has been found

Metastasis refers to the process of cancer cells leaving primary tumor and spreading to other parts of the body, resulting in more than 90% of cancer deaths. Therefore, improving the treatment choice of patients with metastatic cancer has a significant demand. Thus, researchers conduct various studies using recombinant proteins like recombinant horse proteins to get more information.

In order to make cancer metastase, cell death pathways needs to be cut off and the defects of cellular energy production should be changed. The researchers specifically investigated the Ras mutation. Ras gene is a proto-oncogene, which means that it is present in the genes of normal and non-cancerous cells. When Ras DNA shows specific changes or mutations, this mutation can lead to cancer development. Ras mutations are most common in lung cancer, colon cancer and pancreatic cancer. Ras is the most common mutated oncogenes which are observed in all human cancers.

"We found that for cancer cells with Ras mutations, it can turn off cell death pathways by adjusting two different proteins: SGK-1 and PHLPP1," Schaefer said, "We found that cancer cells containing Ras mutations lack for adsorption to cellular extracellular matrix, and adsorption of cancer cells in metastasis is also low. It activates SGK-1 protein, which results in an increase in energy production. The improvement of energy increases the survival of these cells. At the same time, Ras also causes the decrease of number of PHLPP1 protein. Therefore, the ability of PHLPP1 causing cell death is reduced. In general, these changes (SGK-1 activation and PHLPP1 reduction) of cells promote the survival of the metastasizing cancer cells."

Although more research needs to be done, the study results show that an effective strategy of using Ras mutation to eliminate cancer metastasis may simultaneously inhibit SGK-1 activity, thereby blocking the production of energy and restoring PHLPP1 activity, leading to cell death.

"We are currently expanding our research to better understand whether PHLPP1 and SGK-1 play an important role in cancer cell aspects of different stages of the control of cancer cell metastasis." Schaefer said.

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The growth of abdominal aortic aneurysm may be inhibited by the tea polyphenol in green tea

A research team at Kyoto University announced in August 18, 2016 that they demonstrated through mice experiments that tea polyphenol in green tea can prevent the spread and magnification of abdominal aortic aneurysm. Researchers from Kyoto University accomplished the experiments using recombinant mouse proteins, and detailed findings have been published in the renowned medical journal Journal of Vascular Surgery on July 26th.

Once abdominal aortic aneurysm is ruptured, the mortality of a patient is more than 50%. During the period from the onset to the tumor rupture, the patients often show no noticeable symptoms, so it is difficult to detect. The larger the diameter of tumor is, the higher the risk of rupture is.

In this study, the team members divided the mice with abdominal aortic aneurysm into two groups. In two weeks' time, one group was provided with normal drinking water, while another group was provided with drinking water mixed with green tea with tea polyphenol. Two weeks later, through serving elastase and other substances, they established experimental mice models of abdominal aortic aneurysm.

Through four weeks' observation after the establishment of models, the researchers found that compared with the group served with normal drinking water, the group served with drinking water containing green tea polyphenol, the growth of abdominal aortic aneurysm was significantly suppressed. Besides, green tea polyphenol also promotes the synthesis of elastin. Elastin is the main component protein of aorta wall, and the increased content of makes abdominal aortic aneurysm difficult to break. The researchers confirmed that inflammation caused by abdominal aortic aneurysm was also suppressed. Although excessive intake of green tea polyphenol may cause liver dysfunction, the amount of this experiment didn't cause the adverse effects.

Green tea polyphenol has a physiological role in inflammatory and anti-oxidation and can play a preventive effect on cancer and cardiovascular disease. Researchers at Kyoto University said the results of this study show the possibility of effect of green tea on human health and life extension. Flarebio provides recombinant proteins of good quality like recombinant NRG3 at competitive prices.

Exclusive use of a small molecule drug shows good effect on liver repair

Chinese researchers said on 17th that a small molecule drug will promote the repair and regeneration of damaged liver and it has achieved excellent therapeutic effect in mice experiments using recombinant mouse proteins.

The study is published in the new issue of the US journal Science Translational Medicine. One of the study leader, vice president and Professor Zhou Dawang of School of Life Sciences in Xiamen University said, "Previous studies of promoting repair and regeneration of tissues pay more attention to complex treatment strategies on delivering biological materials to the certain sites, while this research showed that exclusive use of the small molecule drugs are expected to promote the repair and regeneration of the liver.

The research of Professor Zhou, professor Deng Xianming from Xiamen University and Professor Yun Caihong at Peking University is focused on the Hippo signaling pathway which can regulate human organ regeneration and size. Previous studies have shown that a kind of protein kinase called Mst1 / 2 in this signal pathway prevents the continuous regeneration of multiple tissues including liver, so they wanted to develop drugs to inhibit such protein kinases. Finally they found a small molecule inhibitor and named it XMU-MP-1, a chemical drug.

Their study showed that the drug not only has made significant activity in protein and cellular level, but also has achieved excellent therapeutic effect in mouse models with tissue injuries such as acute liver injury caused by liver resection blade and the drug Tylenol. It can effectively improve the rate of liver regeneration initial stage and significantly reduce mortality in acute liver injury and so on.

In addition to liver, the drug also can be used for the repair and regeneration of the intestinal tract. The researchers said this study is the new exploration of new kinase-targeted drugs in the therapeutic field of promoting tissue regeneration and repair and has gained attention of some pharmaceutical companies. Flarebio offers recombinant proteins of good quality, such as recombinant Cdh5.

Plant chemical that determines a honey bee's caste has been found

A study was reported in the journal Science Advances shows that broad developmental changes occur when honey bee larvae are switched from eating royal jelly to a diet of jelly that includes honey and beebread, which is a type of processed pollen. Beebread and honey contain p-coumaric acid, but royal jelly does not. Queens feed exclusively on royal jelly. Worker bees known as nurses feed the larvae according to the needs of the hive. The study also used some recombinant proteins to achieve some results.

Experiments revealed that ingesting p-coumaric acid pushes the honey bee larvae down a different developmental pathway from those fed only royal jelly. Some genes, about a third of the honey bee genome, are upregulated and another third are downregulated, changing the landscape of proteins available to help fight disease or develop the bees' reproductive parts.

"Consuming the phytochemical p-coumaric acid, which is ubiquitous in beebread and honey, alters the expression of a whole suite of genes involved in caste determination," said University of Illinois entomology professor and department head May Berenbaum, who conducted the study with research scientist Wenfu Mao and cell and developmental biology professor Mary Schuler.

According to May Berenbaum, compared with the question of what components in royal jelly lead to queen development for many years, what might be more important is which plant chemicals that can interfere with development.

"While previous molecular studies have provided simple snapshots of the gene transcript variations that are associated with the exposure of insects to natural and synthetic chemicals, the genomics approaches used in this study offer a significantly more complex perspective on the biochemical and physiological processes occurring in plant-insect interactions," said Schuler.

This research about how honey bee colonies determine which larvae will serve as workers and which will become queens shows that a plant chemical, p-coumaric acid, plays a key role in the bees' developmental fate. Flarebio provides you with superior recombinant proteins like recombinant CDH11 at good prices.

Developing more effective and tailored therapeutic approaches for managing IBD

Theresa Alenghat, VMD, PhD, from Cincinnati Children's Hospital Medical Center, OH, was awarded with the 2015 AGA-CCFA-Janssen Research Award in Inflammatory Bowel Disease (IBD) Epigenetics Research, which means that Dr. Alenghat who are interested in producing recombinant proteins including recombinant horse proteins, as the inaugural recipient of this award, will receive $100,000 per year for three years to study the role of epigenetics in the development of IBD.

Epigenetics -- referring to modifications of DNA and DNA-associated proteins due to any number of patient and environmental factors -- is an active area of research in IBD and a wide range of other diseases. The promise of epigenetics comes from the knowledge that epigenomic changes regulate gene expression in response to environmental triggers without altering the genetic sequence. Therefore, epigenetics represent an important, potentially reversible, target for IBD treatments.

With the grant, Dr. Alenghat will have the resources to conduct both basic and translational research initiatives to test how bacteria trigger changes in the epigenome during the development of IBD. Dr. Alenghat serves as assistant professor in the division of immunobiology at Cincinnati Children's Hospital Medical Center. "These novel insights may guide the development of more effective and tailored therapeutic approaches for managing IBD," said Dr. Alenghat.

Specifically, Dr. Alenghat will be testing the hypothesis that dysregulation of epigenomic modifications, in combination with alterations in the microbiota, drive the development and progression of IBD.

Crohn's disease and ulcerative colitis are painful and medically incurable illnesses that attack the digestive system. The former one may attack anywhere along the digestive tract (mouth to anus), while the other one only occurs in the large intestine (colon). Symptoms may include abdominal pain, persistent diarrhea, rectal bleeding, fever, fatigue and weight loss. More than 1.6 million Americans live with Crohn's disease and ulcerative colitis, the two diseases that fall under the IBD umbrella. Many of them require hospitalization and surgery. What's worse, these illnesses can cause severe complications, including colon cancer in patients with long-term disease.

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Researchers first draw the map of human body generating different antibodies

Researchers at Stanford University draw the map of human body generating different antibodies for the first time, revealing that different cells which generate antibodies all are derived from a single progenitor cell. This 8-person research team was led by Horns' mentor (bioengineering professor Stephen Quake at Stanford University). He believes that the comprehensive understanding of body's natural defense mechanisms can allow researchers to find new treatments in many different immunological disorders using recombinant human proteins.

The researchers extracted B cells from the blood samples of 22 healthy young adults and made use of high-throughput gene sequencing to obtain the gene sequence of B cells producing antibodies and established a large antibody gene library. By a variety of analytical techniques, researchers identified different types of antibodies. In the cells analyzed by the study group, about three quarters of the cells generated IgM antibody ((Immunoglobulin M).

IgM is "the default type of all antibodies when they are born". When they are activated by immune stress, class switching would happen. A majority of IgM cells would generate to IgG antibody (Immunoglobulin G), and IgG antibodies are the most important fighters against viruses. These cells would further form four kinds of IgG subtypes which all have specific anti-viral properties. A small number of IgM cells would generate into IgA (Immunoglobulin A) antibodies, and IgA can resist the invasion of cells and also help to maintain a healthy balance of beneficial bacteria in the digestive tract. Very few IgM cells would generate into IgE (Immunoglobulin E) antibodies which can cause the body's inflammatory response; if overactive, it can also cause allergic reactions.

Horns' thought of cell type switching process will provide a series of new therapies for immune disorders diseases. Next, Horns plans to conduct sequence for patients with immune system disorders to identify differences in antibody generation and Horns reference chart, thus stepping an important step in developing drug therapy of restoring balance of antibodies. Flarebio provides you with recombinant proteins of good quality, such as recombinant ITGB2.

The effect of Metformin + empagliflozin is better than any single drug

According to a study published online on August 4th in the journal Diabetes Care, compared with taking empagliflozin once a day or taking metformin once every two days, taking empagliflozin + metformin for 24 weeks can more significantly reduce glycated hemoglobin (HbA1c). The research used a lot of recombinant dog proteins.

MD and Ph.D Samy Hadjadj from Central Hospital of University of Poitiers in France and his colleagues randomly assigned 1,364 naïve patients with type 2 diabetes treatment drugs of empagliflozin + metformin, empagliflozin, metformin for 24 weeks. The authors studied glycated hemoglobin change from baseline to 24 weeks.

In the first 24 weeks, the researchers observed that for participants who took part in the treatment regimen of taking empagliflozin + metformin twice daily, glycated hemoglobin decreased 1.9 to 2.1 percentage points; for participants taking empagliflozin once daily, it decreased by 1.4%; for participants taking metformin twice daily, it went down by 1.2 to 1.8 percentage points. Compared with treatment regimen of taking empagliflozin once daily (P <0.001 ) and taking metformin twice daily (P <0.01 < span = "">), the regimen of taking Empagliflozin + metformin twice daily with was related to significant reduce of HbA1c. After 24 weeks, regimen of metformin twice daily and empagliflozin + metformin twice daily treatment were more correlated (P values were <0.001 ) to the weight loss of patients. In the entire group, the incidence of adverse events was similar.

"The period of Empagliflozin + metformin twice daily therapy is 24 weeks. For newly-diagnosed diabetics, it can significantly reduce glycosylated hemoglobin and is superior to taking empagliflozin once daily or metformin twice daily. It doesn't increase the risk of hypoglycemia but reduces weight and shows well tolerance." the authors wrote. Flarebio offers recombinant proteins of good quality, such as recombinant Pigr.

Predicting metabolic pathway of protein interactions is still a challenging task

Cellular activity is subject to physical property and function of several proteins which are involved in a variety of biological pathways. By practicality of genome sequencing and high-throughput experimental data, researchers can make use of a variety of computer technologies and recombinant proteins such as recombinant rat proteins to identify the interaction among whole-genome proteins. The comparative assessment technologies of predicting protein-protein interactions have frequent reports in the literature, but they still have no ability to explain a specific biological pathway.

Methods: In order to learn the ability of predicting the interaction among proteins in specific biological pathways, our report is based on analysis of biological pathways of fourteen E. coli cataloged in KEGG database. The database uses the prediction method of protein function link. These methods are simple phylogenetic appearance surgery (phylogenetic profile), adjacent to the gene, ortholog coexist in the same gene cluster, a mirrortree variants and expression similarity.

Conclusion: Our results show that the predicting metabolic pathway of protein interactions is still a challenging task, and some of the methods may reflect the flexible / independent evolutionary history of proteins. These methods have forecasted that function-related proteins involving amino acids, nucleotides, polysaccharides, vitamins and coenzymes family pathway is superior than the random mechanism related to carbohydrates, lipids and energy metabolism. We also conducted similar observation on the interaction among proteins which is associated with environmental information processing.

On the contrary, genetic information processing and special processes which happen in the subset of organisms and are related to sporty proteins link are predicted with relatively-high accuracy. Given the racial pattern as a good enough method to reconstruct the central dogma of protein-protein interactions between the pathways, metabolic pathways are most easily to be predicted using orthologous group neighboring. If not based on a specific pathway, then the similarity method of gene expression is the best choice. Flarebio provides you with good-quality recombinant proteins including recombinant App at good prices.

Circadian rhythm and virus infection may affect the process of disease

A study suggests that the relation between time of virus infection and circadian rhythm of the host may affect the process of disease. Interfering circadian rhythm of an organism may affect its immune response, but the impact of host circadian rhythms on virus process remains unclear. Thus, researchers in this study decided to use various recombinant proteins such as recombinant mouse proteins to descend into the problem.

Akhilesh Reddy and his colleagues used a herpes virus to infect mice and mice fibroblast cells at different times of a day. When compared with mice infected with the corresponding matt active phase, mice which were corresponding to light phase in the rest period and beginning to expose to these viruses showed a 10-fold virus replication.

Similarly, the time of infection affects virus replication of the fibroblasts cells in mice, suggesting that the cells rhythm clock controls viral process. In addition, interfering the key clock gene Bmal1 can increase the herpes infections of mice and mice fibroblasts and also increase the A influenza virus infection of mice fibroblasts.

Proteomics analysis showed that intracellular protein transport, biosynthesis, protein synthesis and chromatin assembly may affect such rhythm regulation of viral infections. According to the authors, these findings suggest that interfering rhythm cycle may affect the severity of virus infection and may represent a potential tool for the regulation of viral replication in the host.

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Scientists discover the regulatory role of LSD1 in somatic cell reprogramming process

Recently, the journal Scientific Reports published the latest research results of Zheng Hui study group from Guangzhou Institute of Biomedicine and Health and Chinese Academy of Sciences online, and the paper is titled "Lysine-specific histone demethylase 1 inhibition promotes reprogramming by facilitating the expression of exogenous transcriptional factors and metabolic switch". The research, using various recombinant proteins including recombinant horse proteins, reveals the regulation mechanism of histone lysine residues methylation enzyme LSD1 on cell metabolism and the transcription factor expression in somatic cell reprogramming process.

Epigenetic refers to heritable changing process of gene expression the process of cell division without altering DNA sequence. While in the process of cell reprogramming, epigenetic information within cells has changed, and especially histone methyl glycosylation state has undergone tremendous changes. As a member of epigenetic modification enzymes, LSD1 can specifically modify histone lysine residues H3K4 and H3K9 methylation status, but the study reports of its mechanism in the reprogramming process are relatively less.

Zheng Hui study group used MEFs and pre-iPSCs cells as model system to systematically describe the gene expression of LSD1 to exogenous transcription factors in reprogramming process and its impact on the transformation of metabolic way in reprogramming process. The researchers found that in the reprogramming process of somatic cells, inhibiting the activity of LSD1 can improve the efficiency of cell reprogramming. Further study found that inhibiting the activity of LSD1 can prevent the H3K4 demethylation of upstream area of exogenous transcription factor gene, thereby improving the expression of endogenous transcription factor, but also speed up the transformation of metabolic way in reprogramming process by affecting the expression of Hif1α gene and its downstream genes, thus improving the efficiency of reprogramming process. Finally, in the process of pre-iPS cells transforming into iPS cells, inhibiting the activity of LSD1 also can significantly improve the conversion efficiency of the pre-iPS cells by changing their metabolism way.

The research was mainly conducted by Zheng Hui study group and Guo Yunqian from Beijing Forestry University. Related achievements were funded by the National Natural Science Foundation of China, Chinese Academy of Sciences, Municipal and Technology project of Guangzhou. Flarebio provides you with good-quality recombinant proteins such as recombinant ACSL3 at competitive prices.

To block some micropores of HIV to make the viruses to lose their ability of self-replication

Scientists from the University of Cambridge at London and the Royal College of England successfully suppressed the reproduction of HIV by freezing the pores of protein coat. Viruses construct infectious DNA through these pores. The biologists published the relevant reports in the journal Nature. It is worth mentioning that there is already a kind of recombinant human proteins in the market which have entered clinical stage.

HIV belongs to the retrovirus. To infect cells, it must convert the RNA which forms its genes into DNA. However, scientists do not know how virus obtains the necessary nucleotide - the cornerstone of the genetic materials. In addition, they don't know how HIV successfully protects their DNA from the protection system.

The researchers studied the molecular structure of the capsid - viral coat which is composed of proteins. In addition, virologists have created a mutant version of HIV which is used to understand how changes in the capsid affect its ability to infect. Facts have proved that there are special pores in the coat, which are shaped like a diaphragm. Nucleotides enter interior through them, including other foreign molecules which are responsible for identifying foreign DNA. When scientists blocked the micropores using Hexabromobenzene, the viruses lost their ability of self-replication.

The researchers stressed that the inhibitor they tested can't permeate into the cells through plasma membrane. However, they hope to be able to solve this problem and create effective drugs against HIV in the future. In this case, the virus can't multiply and inhibit the activity of immune system, helping to prevent the infection to develop AIDS.

HIV is a virus which causes human immunodeficiency. In 1983, the human immunodeficiency virus was first discovered in the United States. It is a lentivirus which infects human immune system cells. Flarebio offers you with recombinant proteins including recombinant Insr at reasonable prices.

Researchers find two Zika virus proteins related to microcephaly

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

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

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

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

Knocking out a target can improve effect of cancer drugs

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

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

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

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

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

New ultra-fast algorithm makes biochemical and biomedical research speed 10 times faster

According to a new report, a professor from Innopolis University in Russia and scientists from the United States and France worked together to invent an ultra-fast algorithm of protein interaction modeling, which can make biochemical and biomedical research speed 10 times faster. The research used a lot of recombinant proteins.

One of the researchers Holo Dorf said, "The team of scientists from Russia, the United States and France successfully invented this protein interaction modeling. This method is dozens of times faster than similar computing system which is established on the basis of the interaction between two proteins."

Holo Dorf also said that there are dozens of kinds of computer systems used to calculate the interactions between proteins, but these systems are not suitable for the simultaneous simulation of a large number of interactions between proteins. The new method is able to do this. What's more, using the new method enables us to increase the calculation speed by 10 times to 100 times. The accuracy of the calculation results are not affected at the same time.

Scientists are currently working to develop drugs which can act directly on diseased cells without any side effects. Proteins are the most basic materials of the cells, while drugs will interact with the proteins in the body. To develop effective drugs without any side effects, we must study the interaction of different proteins and their characteristics in the human body.

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The susceptibility of sarcoma may be increased by some oncogenes

A recent study published in the journal Lancet Oncology showed that the germline mutations of some known oncogene may increase the susceptibility of sarcoma for individuals. Sarcoma is a rare bone and soft tissue cancer. An international team led by Australian researchers conducted targeted gene panel sequencing on more than 1,000 patients with sarcoma. In addition to known mutations associated with sarcoma, the sequence data also revealed that other types of genes related to cancer showed recurrent mutations, such as TP53, ERCC2, ATR, BRCA2 and ATM.

The researchers found that in these patients who received tests, more than half of them carried at least one mutation in cancer-related genes, and people who carrying a plurality of cancer-related mutations in genes showed increased risk of arly-onset sarcoma. They accounted for 1/5 of the people who received the test.

Corresponding author of the article DavidThomas said, "The combination of influence of various genes combined increased risk of sarcoma. More mutations a patient carry, cancer comes sooner. Previously we can't judge the populations and family at risk, but now we can better manage this risk and help these people to be treated in time of need."

Thomas and his colleagues focused on 72 potential genes with cancer risk and extracted extract DNA of blood or saliva samples of 1,162 sarcoma patients aged above 15 and conducted targeted gene panel sequencing. About 3/4 of the people are Caucasian, and about 15% of them with multiple primary cancer.

Researchers compared the control groups and found that about 55% of patients with sarcoma showed suspicious increase of germline mutations, and these variations appeared to be pathogenicity. Mutations mostly happened in TP53, BRCA2, ATM, ATR and ERCC2 genes.

The research team plans to continue to expand the current research results to conduct whole genome sequencing on the sample of people with risk of germline sarcoma.

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Scientists find a gene that controls the production of stem cells

When talking about stem cells, it seems hard to judge them. If too many new stem cells are produced, it may lead to cancer, while too few would inhibit the repair and maintenance of the body.

Good news comes here. USC researchers In Kyoung Mah from the lab of Francesca Mariani and colleagues at the University of California, San Diego, (UCSD) published a paper in the Stem Cell Reports. They describe a key gene in maintaining this critical balance between the results of producing too many and too few stem cells. The gene is called Prkci. It influences whether stem cells self-renew to produce more stem cells, or differentiate into more specialized cell types, such as blood or nerves.

The team conducted experiments by growing mouse embryonic stem cells, which lacked Prkci, into embryo-like structures in the lab. Without Prkci, the stem cells preferred self-renewal, and generated large numbers of stem cells, thus producing an abundance of secondary structures.

After careful inspection, the researchers found that stem cells lacking Prkci had many activated genes typical of stem cells, and some activated genes typical of cardiac, neural, and blood-forming cells. As a consequence, the loss of Prkci can also motivate stem cells to differentiate into the progenitor cells that form neurons, blood and heart muscle.

Prkci activates or deactivates a well-known group of interacting genes that are part of the "Notch signaling pathway to achieve the effects mentioned above. When Prkri is absent, the Notch pathway would produce a protein that signals to stem cells to make more stem cells. When Prkri is present, the Notch pathway just keeps silent and the stem cells all differentiate into specific cell types.

Their findings are good cues for the development of patient therapies. For example, patients with certain injuries or diseases may be benefit from them by using small molecule inhibitors to block the activity of Prkci, thus improve stem cell production. It will be wonderful to apply the findings to the case where stem cells are hard to generate.

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New understanding of the treatment of sickle cell disease

An international team of researchers found a new biophysical marker which can help to improve the awareness of the treatment of sickle cell disease, taking an important step to treat the inherited blood disease. Each year, about 80,000 to 100,000 Americans suffer from the disease. The results will be published online this week in the early version of Progress of National Academy (PNAS), which also has many other studies on recombinant proteins.

Patients with hemoglobin shape sickle cell disease show abnormal shape of hemoglobin. Hemoglobin is protein used by red cells in vivo to carry oxygen. The shape of normal red blood cells is biconcave disc-shaped and is easy to deform and stretch, which is easy to get through narrow blood vessels of the body. In sickle cell disease, abnormal hemoglobin forms fibers. When under the condition of hypoxia, it will lead red blood cells to become flattened, sickle-shaped or harden. The change in shape and hardness can make red blood cells be stuck in the blood vessels, preventing oxygen to be transported to the surrounding tissues. This can cause anemia and extreme pain, affecting the health of body tissues and organs.

Currently, hydroxyurea is the only drug approved by FDA for the treatment of sickle cell disease. The drug improves sickle of red blood cells and is used for the treatment of pain and alleviating the need of blood transfusions for some patients, but it is not effective in all patients. Researchers have long debated what the mechanism of the drug is. So they have conducted a lot of research using recombinant rat proteins.

In the current study, the international team evaluated the biophysical properties of red blood cells - the shape, surface area and volume, biomechanical properties - flexibility and viscosity under normal oxygen conditions and used electromagnetic waves to measure small differences in the physical properties. This technology is known as the common path interferometric microscope, which allows researchers to obtain three-dimensional images of the cells.

The researchers took blood samples from patients with sickle cell disease and divided them into four groups based on the density of red blood cells. The density of normal, disk-shaped red blood cells is minimum, while density of severe sickle cells is maximum. Then they collected blood samples of patients who received hydroxyurea treatment and not. Red blood cells of patients who received treatment showed improvement in physical and biological properties. In addition, physical properties-related red blood cells of patients receiving treatment is greatly related to erythrocytes compared with the level of fetal hemoglobin.

The researchers hope that these biophysical markers can be combined with biochemical and molecular markers to assess the severity of the suffering degree of patients to determine whether hydroxyurea therapy is effective and to monitor the effects of the treatment. Flarebio provides recombinant proteins such as recombinant ITGB2 at good prices.

JAM-C protein is expected to become a new target for lymphoma therapy

Lymphocytes are the key components of immune system, and they can remove invading pathogens or cancer cells and other "apostate". However, like other cells, they themselves may become cancer cells due to a genetic mutation, causing lymphomas. On the other hand, although largely existing in the blood, only transferring out of blood and entering into lymphatic system (i.e. homing) can lymphoma cells really become dangerous. Scientists made use of various kinds of recombinant proteins such as recombinant dog proteins and recombinant rat proteins to study it.

"Because lymphoma cells can't survive in blood for a long time, these must find a more suitable living environment - such as the lymphatic system - and continue to amplify. While we need to limit them in the blood to prevent them to cause harm," said Professor Thomas Matthes at the University of Geneva, Switzerland.

The key lies in a junctional adhesion molecule JAM-C. This protein is expressed on the surface of a variety of cells in the human body, including normal B lymphocytes and some B-cell lymphoma cell subtypes, such as diffuse large B-cell lymphoma (MCL). Furthermore, JAM-C protein is also expressed on the surface of endothelial cells so that JAM-C protein on the lymphoma cell can conduct it affinity recognition, thus allowing the above-described cell lymphoma to freely get through the vessel wall and transfer to adjacent lymphatic system.

Professor Thomas Matthes team developed a monoclonal antibody H225 of JAM-C protein. In the mouse model of lymphoma, they found that H225 can effectively curb the homing process of JAM-C-positive lymphoma cells to reduce the incidence of the latter by half. The results were published recently in the Journal of Leukocyte Biology.

Moreover, even after transferring to the bone marrow, spleen, lymph nodes, liver and other organs, the amplification of JAM-C-positive lymphoma cells is still suppressed by H225. In mice research, H225 almost completely cleared tumor cells of the above organs. Further research found that H225 inhibits the phosphorylation of ERK1 / 2 kinase in JAM-C-positive B cells and MAPK signaling pathway which belongs to it without affecting other signaling pathways. This is the first time to discover in JAM-C-positive B cells that MAPK signaling pathway can be activated by JAM-C. Thus, the role of H225 is likely not limited to preventing lymphoma cell form homing.

Currently, researchers are working hard to develop this discovery into lymphoma therapy which can be used in clinic. JAM-C is expected to become a new target for lymphoma therapy to achieve inhibition of lymphoma cell expansion and create a tumor microenvironment which is beneficial to the treatment. Flarebio offers superior recombinant proteins including recombinant CDH2 at good prices.

Protein in hake's eyes becomes new hope for people with corneal blindness

Corneal blindness is a visual impairment which affects about 10 million people in the worldwide. It occurs from the cornea becoming clouded, scarred or any other infection that ultimately affects the transparency of cornea, finally making a person blind. It includes a range of eye diseases, injuries or infections that damage the corneal tissues and lead to permanent blindness. Due to shortage of cornea donation, only 100,000 can receive transplantation each year. Now researchers have new findings in research using recombinant human proteins.

A recent study at the University of Auckland in New Zealand found that they can make use of a kind of protein in the eyes of hake to make alternatives of human cornea. The study is expected to solve the shortage of donated corneas.

Researchers from Auckland University said they can get rich protein from the eyes of hake and use them to create biological materials for "corneal tissue engineering" of human beings, namely manufacturing cornea alternatives.

Medical director and leading ophthalmologist from Focus London clinic Alam said, "This news brings new hope for thousands of people who are at the risk of blindness. In a recent trial in UK, doctors first used IOL (intraocular lens) to conduct transplantation. This is really encouraging news. However, the synthesis technology is still in its infancy, and the operation is expected to begin in 2017. If the eye crystals of the fish prove to be effective, it can change the fate of thousands of people in this country and around the world."

Biological Sciences researchers from University of Auckland said that the possibility of such transplant having rejection is very small. Flarebio Biotech LLC offers good-quality recombinant proteins including recombinant LARGE at good prices.

Cancer cells: the new discovery of PITPNC1 protein

Researchers from Rockefeller University at New York and the University of Bergen at Norway published their discovery of a protein called PITPNC1 on the journal Cancer. Molecular biologist at the University of Bergen, first author Dr. Nils Halberg who is interested in producing recombinant proteins like recombinant dog proteins said, "We found that invasive cancer cells spreading in colon, breast and skin cancer have higher content of PITPNC1 protein than non-invasive cancer cells."

More than 90% of cancer deaths are due to metastasis, namely so-called new tumor lesions caused by the condition that invasive cells leave the primary tumor and metastases to other parts of the body. Any discoveries about the metastasis process of cancer cells all help us step further on the way of saving millions of lives.

The name of metastatic cancer cells is the same with that of the cancer cells it comes from. For example, lung metastatic cancer forming by a kind of breast tumor metastasis is known as metastatic breast cancer, instead of lung cancer. Under a microscope, metastatic tumor cells generally look very similar to primary cancer cells. Moreover, metastasis cancer cells and primary cancer cells often have some similar molecular features, such as the expression of certain proteins. It can be proved by many recombinant proteins such as recombinant rat proteins.

Dr. Halberg explained that there are many different kinds of cells inside a tumor cell. Some of the cells are benign and will not cause any troubles, while some cells become invasive and are ready to spread at any time. And it is difficult to predict which cells are about to become invasive cells.

In their paper, the team describes how they separated invasive cells from the metastatic breast cancer, melanoma and colon cancer and how they found that the invasive cells all express a kind of genes more highly than cells without proliferation. The gene encodes the protein PITPNC1. Dr. Halberg said, "This means that we can make a forecast about which tumor cells are easy to become invasive and spread at an earlier stage than what we can do currently."

He and his colleagues also found that this protein also has a very specific function in the process of cancer spread. It can make of blood vessels to metastase tumor cells to new sites in vivo. In order to be able to leave the tumor and enter blood vessels and then adhere to a new organ, invasive cells need to penetrate tissue. Dr. Halberg said that they cut matrix proteins around cells by releasing a kind of molecules like scissors, while it is PITPNC1 protein which regulates this process.

The team hopes that the results would help to find treatment to reduce the risk of proliferation of cancer - for example, after surgery. Halberg concluded, "If we can provide a personalized treatment targeting at this protein, we can prevent the spread of it."

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Nature: toremifene is expected to be an anti-Ebola drug

Fatal infections caused by Ebola virus (EBOV) break out frequently in recent years, and Ebola outbreak in West Africa caused a large number of deaths. There are no approved effective drugs or vaccines against EBOV. Since 2013, scientists have adopted a large number of small molecules and marketed drugs in vitro mouse model tests and computer virtual screening to find compounds of anti EBOV. In 2013, Johansen, LM et al., conducted experiments on a series of selective estrogen receptor modulators including anticancer drug toremifene, finding that they have potential inhibitory effect on EBOV virus. But they did not clarify the mechanism.

Recently, David I. Stuart and other researchers from the University of Oxford took EBOV outer membrane glycoprotein (GP) as the study object and found that toremifene can combine GP and reduce its stability, thereby blocking viral fusion with the endosomal membrane and playing anti-viral effect. They also resolved the crystal structure of GP protein and the complex of GP protein, toremifene and ibuprofen, clarifying the action mechanism of toremifene.

EBOV outer membrane has a three-glycoproteins (GP, furin protein is cut into two subunits GP1 and GP2), which is solely responsible for host cell attachment, fusion kernel entry and film. Thus, GP is the primary target for the development of antiviral drugs. The researchers used recombinant protein - recombinant EBOV outer membrane glycoprotein (GP) to test whether the nine compounds would bind directly to proteins through the method of protein thermal transfer. Experimental results showed that when the dose of toremifene was 100 μM and pH value was 5.2, it can significantly reduce the melting temperature (Tm) of EBOV GP to 14 ℃. This is opposite to the previously-reported research result that inhibitors reducing the melting temperature of proteins will increase the stability of protein structure. In contrast, ibuprofen showed only a very critical effect (Tm decrease rate was less than 2 ℃), lacking for potential virus inhibition.

The researchers also first reported EBOV GP protein with no ligand and high-resolution crystal structure of the GP and toremifene and ibuprofen complex. Surprisingly, toremifene and ibuprofen all combined in a hole between the subunits GP1 and GP2. This hole is located in a huge tunnel entrance, and this big tunnel can be connected with other similar tunnels. The interactions of drug and GP1, GP2 are mainly hydrophobic effect. In filamentous virus, amino acid residues which combine with these drugs are highly conserved, excepting Marburg virus (MARV), indicating that the Marburg virus probably will not be combined with these drugs. This work illustrates the suppression mechanism of drugs on viruses, providing a viable direction for the development of more anti-EBOV drugs. Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. And high-quality recombinant proteins such as recombinant NRG3 are offered at competitive prices.

New study provides theoretical basis for the treatment of inflammatory related diseases

Zhang Haibing Study Group at Institute for Nutritional Sciences, SIBS, Chinese Academy of Sciences reveals the functional mechanism of programmed cell death-associated protein MLKL and FADD in inhibiting lymphocyte proliferation and activation of inflammatory body NLRP3, providing theoretical basis and new ideas for the treatment of inflammatory related diseases. Related research was recently published online in the journal Cell-Communication, which also provides many studies on recombinant horse proteins.

FADD is an important molecule which mediates apoptosis. Mice with FADD knockout died in about 11.5 days in embryonic stage, but simultaneous knockout of RIP3 could save embryonic lethality, and mice with FADD and RIP3 double knockout showed progressive proliferation of lymphocytes.

The researchers used CRISPR / Cas9 system to build mice with FADD and MLKL double knockout, first confirming that MLKL deletion can save FADD knockout-caused embryonic lethality. Further studies showed that with age, mice with FADD and MLKL double knockout began to suffer from systemic autoimmune lymphoproliferative disease at about the age of 9 weeks, manifesting as generalized lymphadenopathy and splenomegaly. Flow analysis showed that the accumulation of a large number of CD3 + B220 + double-positive lymphocytes existed in the lymph nodes and spleen of mice, and it increased with the development of the disease.

At the same time, studies showed that in the conditions of MLKL and FADD commonly missing, bone marrow macrophages NF-kB signaling pathway weakened, reducing the transcription of key molecule NLRP3 which was dependent by inflammation body activation, thereby affecting the formation of inflammatory body, the cut of Caspase-1 and the secretion of IL-1β.

The study reveals the regulation mechanism of FADD and MLKL in the process of mouse embryonic development, immune system balance homeostasis and inflammatory body activation, providing new evidence for cell death related proteins involving in inflammation reaction as well as potential drug targets for the treatment of inflammatory diseases. Flarebio offers recombinant proteins such as recombinant ACSL3 at good prices.

The study of female germline stem cells has achieved new progress

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

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

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

The great advantages of prokaryotic expression system for recombinant proteins

Prokaryotic expression system is developing well and the process is simple and fast. It has the advantages of low cost and high yield and is worthy trying for most proteins. It is especially suitable for eukaryotic proteins which express prokaryotic sources and don't require post-translational modification.

The necessary host bacteria of prokaryotic expression system include E.coli, Bacillus and the like. Wherein the Gram-positive Bacillus is more suitable to secrete and express recombinant proteins such as recombinant human proteins in its periplasmic space; gram-negative E.coli is capable of expressing heterologous proteins at broad spectrum.

E. coli expression system is currently the most developed recombinant protein expression system. Common strains of E. coli include BL21 (DE3), BL21 (DE3) Star, and B834 (DE3) and so on. All these strains were knocked out protease and are lysogenic to phage DE3. DE3 is a derivative λ phage with a phage resistance zone 21 and / ac / gene, / acUV5 promoter and T7 RNA polymerase gene. This section is inserted into the int gene, thus preventing DE3 from integrating into the chromosome or being excised from the chromosome in the absence of helper phage. Once forming DE3 lysogen state, only /acUV5 promoter induced by IPTG guides T7 RNA polymerase gene transcription. Add IPTG-induced T7 RNA polymerase production in lysogen culture system and then target DNA on plasmid begins to transcribe.

At the same time, there are some specially-designed strains expressing recombinant proteins with special needs. For example, methionine auxotroph expresses selenomethionine proteins; strains with enhancement of solubility express toxic protein expression strains; strains supplemented with rare codons express eukaryotic proteins. And here I would recommend a biocompany named Flarebio which produces and provides superior recombinant proteins including recombinant Cdh10 at competitive prices.