Newly-developed technology can directly detect Ebola virus

Ebola virus is such a deadly disease that found in 1976 in Africa. It is an unusual disease and after being discovered, it caused widespread concern and attention within the medical profession. Since 2014, Ebola virus in West Africa has killed over 11,000 people. Recently there are new cases found in Guinea and Sierra Leone.

A group form researchers at UC Santa Cruz has developed chip-based technology for reliable detection of Ebola virus and other viral pathogens. The system used recombinant rat proteins and can be integrated into a simple, portable device to quickly detect Ebola infections and control outbreaks since it uses direct optical detection of vital molecules. Tests have been done and the results show that the system has the sensitivity and specificity needed to provide a viable clinical assay. The results paper was published September 25 in Nature Scientific Reports.

The current Ebola virus detection relies on a method called polymerase chain reaction (PCR) to amplify the virus's genetic material for detection. Because PCR works on DNA molecules and Ebola is an RNA virus, the reverse transcriptase enzyme is used to make DNA copies of the viral RNA prior to PCR amplification and detection. This PCR detection seems to be more complex compared with the new-developed system, and it requires a laboratory setting. The system would detect the nucleic acids directly and achieve a comparable limit of detection to PCR and excellent specificity.

The system combines two small chips, one microfluidic chip for sample preparation and one optofluidic chip for optical detection. Senior author Holger Schmidt, the Kapany Professor of Optoelectronics at UC Santa Cruz and his collaborators have been developing optofluidic chip technology for optical analysis of single molecules as they pass through a tiny fluid-filled channel on the chip for the last ten years. The microfluidic chip for sample processing can be integrated as a second layer next to or on top of the optofluidic chip.

Although the team has not yet able to test the system starting with raw blood samples due to lack of additional sample preparation steps, it is a great step in the process. The scientists are devoting to make the system to detect less dangerous pathogens and do more useful analysis for other diseases. Flarebio provides recombinant proteins of good quality such as recombinant Cdh4.

Bowel inflammation patients can be saved by this protein

A group of researchers first demonstrated the role of stomach cancer-associated protein tyrosine phosphatase (SAP)-1 in the pathogenesis and prevention of Crohn's disease, ulcerative colitis, and other inflammatory bowel disorders. The group was led by Prof. MATOZAKI Takashi and Associate Prof. MURATA Yoji who're interested in study of recombinant human proteins at the Kobe University Graduate School of Medicine Division of Molecular and Cellular Signaling.

Inflammatory bowel diseases are disorders of unknown etiology that are often characterized by abdominal pain, diarrhea, bloody stool, fever, and weight loss. These diseases include Crohn's disease and ulcerative colitis. These symptoms effect too much on patients' daily life and the patients will be pushed at an elevated risk of mortality. And these patients are more likely to be linked with colorectal cancer.

A lot of studies published recently have demonstrated that intestinal epithelial cells are important in regulating bowel inflammation, but the underlying mechanism remains unknown. Before this, the scientists found that SAP-1 localizes to the microvilli of the brush border in gastrointestinal epithelial cells. The transmembrane-type tyrosine phosphatase SAP-1 has an extracellular domain that protrudes into the intestinal lumen and a cytoplasmic domain that mediates tyrosine dephosphorylation of proteins. They showed that SAP-1 ablation in a mouse model of inflammatory bowel disease resulted in a marked increase in the incidence and severity of bowel inflammation, which suggests that SAP-1 plays a protective role against colitis. What's more, carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 20, an intestinal microvillus-specific membrane protein, was identified as the target of SAP-1 tyrosine dephosphorylation. Suppression of CEACAM20 functions via dephosphorylation contributes to preventing colitis. They believe that their findings will drive the development of drugs that target SAP-1 and CEACAM20 to overcome intractable inflammatory bowel diseases by unlocking the anti-inflammatory mechanism of the intestinal epithelial cells.

The future researches of these scientists will be concentrated on taking advantage of the understanding of SAP-1 and CEACAM20 functions to develop new therapeutics for inflammatory bowel disease. Flarebio offers recombinant proteins such as recombinant CDH4 at competitive prices.

Scientists find a gene variation that can increase the mortality of smokers

Previous studies involving recombinant dog proteins have shown that the clustering genetic variation of the nicotinic acetylcholine receptor subunit (CHRNA5-CHRNA3-CHRNB4) on chromosome 15 has a strong association with smoking and the risk of smoking-related disease. CHRNA5-CHRNA3-CHRNB4 includes chronic obstructive pulmonary disease (COPD), peripheral arterial disease and lung cancer.

As multivariate label of CHRNA5-CHRNA3-CHRNB3 cluster, whether rs1051730 (C/T) is associated with changes in incidence and morbidity of smoking-related diseases? In this regard, we analyzed a population-based prospective cohort study (Malmö diet and cancer study).

At baseline, participants were divided into three groups: current smokers (n = 6951), former smokers (n = 8426), and never smokers (n = 9417). They used Cox proportional hazards model to assess the association of rs1051730 and first-time COPD, smoking-related cancers, other cancers and cardiovascular diseases. They also followed the association between rs1051730 and the overall mortality risk from these diseases in the next nearly 14 years.

Data shows that among current smokers, the first COPD, smoking-related cancer, other cancers and cardiovascular diseases respectively showed 480 cases, 852 cases, 810 cases and 1022 cases. There were a total of 1,508 deaths, among which cardiovascular disease, respiratory disease and cancer were respectively 500, 102 and 677 deaths.

The analysis showed that with the increase in the number of T alleles, the overall mortality, COPD and incidence of tobacco-related cancers increased. The association remained after adjustment for smoking. But for people who never smoked, they did not show this connection.

Our data showed that the genetic variation of the CHRNA5-CHRNA3-CHRNB3 cluster is associated with the increase of mortality of smokers, COPD and incidence of tobacco-related cancers. Flarebio provides good-quality recombinant proteins like recombinant ITGB2 at competitive prices.

Drug-resistant bacteria can be treated by certain polypeptide

Medical and health workers may soon be able to develop a drug for refractory abscess bacteria, because these bacteria almost sent about tens of thousands of people to the emergency room.

Researchers from the University of Columbia in British have used a peptide, or a substance called miniprotein, to successfully stop drug-resistant bacteria from producing abscesses or purulent lesions through recombinant human proteins. Such polypeptide impedes their secretion by interfering with the stress response of the bacteria.

Abscess is bacterial-mediated tissue lesion that causes about 3.2 million people to enter the emergency room each year. The reason for this is that these bacteria are resistant to antibiotics and can only be treated by reducing infection and pyogen.

Microbiology professor Bob Hancock at Columbia University said, "Abscesses can happen almost anywhere in the body, and antibiotics are usually ineffective. While the use of polypeptides gives us a new way of thinking, because its mechanism is completely different to that of antibiotics."

Hancock and his colleagues found that the bacteria in the abscess showed a state of stress growth. They used a synthetic peptide called DJK-5 to interfere with the stress response of the bacteria, thus achieving the effect of treating abscesses in mice.

According to the difference of composition structure of the cell wall, bacteria can be divided into Gram-positive and Gram-negative bacteria, and they also resistant to a variety of antibiotics because of the cell wall. However, this peptide has a good effect against Gram-positive bacteria and Gram-negative bacteria. Flarebio offers recombinant proteins of good quality such as recombinant CDH2.

There are two key genes in epidermis that help a plant keep alive

It is known to all that the body of a plant consists of only three tissue systems - the outermost epidermal tissue, the inner tissue, and the vascular tissue. The epidermis is essential in protecting the body of a plant from external stresses, preventing organ fusions, and determining final organ shapes.

Scientists took Arabidopsis as a model plant and conducted a research using recombinant proteins. Then two kinds of genes, ATML1 and PDF2, have been identified to serve as a key factor involved in the formation of the epidermis. However, there were more remained to be researched about the functional importance of these two genes.

Now, Taku Takahashi and his colleagues at Okayama University in collaboration with a group at the University of Tokyo have provided compeling evidence that the two genes are essential for the growth of embryos in Arabidopsis.

They generated the double loss-of-function mutant of ATML1 and PDF2 and found that the complete loss of these two genes resulted in the embryonic arrest before seed germination.

They confirmed that the inhibition of the expression of ATML1 and PDF2 caused a severe defect in epidermis formation and organ fusions in leaves, stems and flowers.

All the findings provide important information to the understanding of how the identity of epidermal cells is established in the plant embryo. They are also benefit to further studies on how a plant body is formed. Flarebio offers superior recombinant proteins such as recombinant App 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.

To teach protein knowledge through playing games

Gamers players defeated the trained scientists to complete an accurate model of a specific protein at full speed in the same biochemical data obtained conditions through a science-based online game Foldit.

"In this way, they can improve research progress and the knowledge of recombinant proteins such as recombinant horse proteins." Co-author of the study, James Bardwell from the University of Michigan Michigan said.

This game involved 469 Foldit players, two highly-trained experts in crystallography, and two computer algorithms to see who can accurately establish YPL067C protein model through translating electron density map. Eventually, gamers united and established the most accurate version through painful trial and error in the protein modeling experience, Stubbs was the first Quebec.

Organizers stated that the game results show competition may be an effective way to educate students about the protein modeling knowledge. Because compared to the traditional way of learning, competition makes this time-consuming process more interesting. And it encourages cooperation.

"We can see that the players learned a lot of knowledge about proteins in the process of playing the game," co-author, Scott Horowitz from University of Michigan Hoorn said, "We spend weeks of time trying to put these into the brains of students, but Foldit players naturally learn them, because this is very interesting."

Even cooler is that organizers say the gamers may have discovered a new protein that may control the formation of plaque, which can bring more understanding of Alzheimer's after in-depth study. New findings have been published in the journal Nature Communications. Flarebio provides you with superior recombinant proteins like recombinant NRG3 at good prices.

Is our memory stored in brain cells?

Studies suggest that memory is likely to be stored in the brain cells. If this conclusion is correct, it will bring major breakthrough for the treatment of post-traumatic stress disorder (PTSD). The main manifestation of patients Post-traumatic stress disorder is that patients will continue to suffer painful memories of the intrusion.

More than a decade ago, scientists began to use a drug called propranolol for the treatment of post-traumatic stress disorder. Propranolol can block the synthesis of some proteins that are essential for long-term memory. Therefore, this drug was thought to prevent new memory from forming. Unfortunately, through research using recombinant human proteins, researcher got that unless taking the drug immediately after the painful event happens, otherwise people will still have unpleasant memories. Recently, studies have shown that when a person recalls a memory, the re-activated connection is not only enhanced, but will temporarily become easier to change - this process is called memory reconsolidation. The use of propranolol can prevent memory reconsolidation and clear the related synapses.

The researchers applied a slight electrical stimulation to the sea hare to make them form the memory of the event and new synapses in brain. Then, they transferred the neurons of sea hare into culture dish and chemically triggered this memory, followed by the application of propranolol.

As with earlier studies, propranolol cleared this memory-related synapse. However, when the memories of these cells were triggered again, the memory was fully recovered within 48 hours. So they guessed that the memory was not completely stored in the synapse.

Scientists carefully checked the neurons and found that although the synapse has been cleared, but the molecular and chemical changes within cells were retained. It may be that these permanent changes leave traces of memory. Another possibility is that memory is encoded by epigenetic modifications in the DNA of cells, and these modifications will affect the way genes are expressed. Researchers are inclined to the latter explanation.

New research has shown that drug therapy is unlikely to drive the painful memory of patients with PTSD, even though it is just getting started. The researchers said, "If you asked me about whether PTSD could treat with drugs two years ago, I would probably answer yes. But now I do not think so. The new discovery that memory is stored in cells may contribute to the treatment of another memory-related disease - Alzheimer's disease. Flarebio offers recombinant proteins of good quality such as recombinant ACSL3.

The mystery of mice recognizing close relatives has been unlocked

You may be curious about why mice can recognize close relatives even some of them have never encountered before. The mystery has been unlocked by researchers from the University of Liverpool through some recombinant dog proteins.

The researchers published a study in Current Biology demonstrating that a species-specific genetic marker called the major urinary protein (MUP), which is detected through the animal's scent, is used by female house mice to select closely related females as nest partners to help look after their offspring. To their astonishment, another scent-based genetic marker, the vertebrate-wide major histocompatibility complex (MHC), is not involved in kin recognition. It was thought to determine how most animals recognize their relatives before.

It proves that animals, including people, tend to cooperating with close relatives because it increases the odds of the genes that they share with relatives being passed to the next generation. Female house mice usually select relatives as nest partners regardless of prior familiarity, but the genetic markers involved in this recognition have proven extremely difficult to identify.

"This work extends far beyond any previous attempt to identify the genetic basis of kin recognition in vertebrates and strongly challenges the current assumption that there is a common kin-recognition mechanism 'inbuilt' into the immune physiology of all vertebrates," said Professor Jane Hurst, from the University's Institute of Integrative Biology and lead author of the study.

The researchers are preparing to investigate if other species have evolved similar genetic markers to recognize their relatives and whether these signals evolve only in species that cooperate with relatives to increase their breeding success.

To understand the importance of social groupings in populations can also have implications for captive breeding programmers and help those animals cooperate better. Flarebio provides good recombinant proteins including recombinant Insr at great prices.

A new diagnostic method has been developed

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

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

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

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

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

The mechanism of YTHDF2 accelerating polyadenylation and degradation of RNA

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

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

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

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

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

A new technology is expected to be an effective means to prevent cancer metastasis

Cancer metastasis is the leading cause of death for patients with breast cancer. Recently, MIT scientists have invented a new technology that is expected to become an effective means of preventing breast cancer. The research used recombinant human proteins and the results are published in the recent issue of journal Nature Communications. This technology uses microRNA (small non-coding RNA) regulation of gene expression to control cancer metastasis.

Professor Natalie Artzi and the lead investigator of the study in Massachusetts Institute of Technology said that this treatment can be used in combination with chemotherapy for the treatment of early breast cancer. "The hypothesis of this treatment is that if the cancer diagnosis is in early stage, then conducting chemotherapy in the treatment of carcinoma and taking specific microRNAs treatment can effectively prevent cancer metastasis," Artzi said.

The regulation role of microRNAs to gene expression is very important for the prevention of cancer metastasis. Recent studies have shown that gene expression regulation disorder caused by single nucleotide polymorphism (SNP) has a significant impact on the level of gene expression, leading to the increase of risk of cancer.

The researchers compared three SNP and assessed the impact of these three SNP on cell motion. The researchers found that one SNP (rs1071738) is related to cancer metastasis. The researchers found that rs1071738 can interfere two binding sites of microRNA (microRNA can regulate gene expression through binding to DNA) - miR-96 and miR-182, thus changing the expression of a protein called Palladin.

Prior studies have shown that Palladin played a key role in the process of metastasis of breast cancer cells and it is also important for cancer cells to invade normal tissues. Thereafter, researchers evaluated Palladin in the laboratory and found that miR-96 and miR-182 can reduce the level of Palladin protein, thus weakening the ability of breast cancer cells invading into normal tissues.

Subsequently, the researchers developed a method to send improved microRNAs into breast lumps. The test results in mice showed that this method can significantly reduce breast cancer metastasis. Flarebio offers recombinant proteins of good quality such as recombinant Cdh10.

Genome sequencing uncovers the adaptability of water bear in extreme environment

Water Bear is a small aquatic animal, also known as tardigrade. The issue of Nature - Communications published an article of latest research results on its genome sequence on September 20th. Through research using recombinant proteins, the study found that a kind of gene in the body of tardigrade, its protein can resist the DNA damage in human-cultured cells. This suggests that this protein which is specific for tardigrades may help cells to resist DNA damage sources.

Tardigrada can survive in extremely stressful environment (including vacuum), but scientists didn't know specifically how it survives in extreme environments. This ability of tardigrada prompted researchers to investigate its genome. The first genome sequencing results show that in the process of evolution of tardigrade, it obtains a large number of genes from other species by horizontal gene transfer (DNA transfer among genomes of different species). However, the rooted reason of tardigrada showing tolerance in extreme environment is still an unsolved mystery.

Takekazu Kunieda and colleagues at the University of Tokyo, Japan, presented to the high-quality genome of water bears which are known to tolerate high-pressure environment, and they found no evidence of large-scale horizontal gene transfer. But compared with flies and worms, the number of genes which are responsible for tolerating high-pressure environment was much more. In addition, they found a protein which binds to DNA and helps to protect cultured human cells from being affected by X-ray radiation, and they believed that the protein is unique for Tardigrada. Through a detailed comparison of tardigrada genes and genes from other species, the authors found that the gene designated as the genetic code of this protective protein may be specific to Tardigrada. These results don't support the viewpoint of the tolerance coming from horizontal gene transfer.

Although it remains unclear how tardigrada's unique adaptability play a role in the molecular level or organism level, the results of the study show that tardigrada has evolved and obtained unique "cheats" against high-pressure condition. Flarebio provides superior recombinant proteins such as recombinant Nrg2 at good prices.

Dormant bacteria may be chief culprit of diseases

Recent DNA sequencing method reveals that, per milliliter of blood contains about 1,000 bacterial cells. These bacteria are usually dormant. But they can be woke up when the blood iron is made use of by bacteria and begin to secrete lipopolysaccharide (LPS). This molecule will cover on the cell wall and the immune system will recognize it and inflammation happens.

Douglas Kell from University of Manchester and Resia Pretorius from University of Pretoria in South Africa wonder whether LPS also directly causes blood clotting. The most of the bacteria which are dormant in the blood come from the intestinal tract. Through research using recombinant dog proteins, the researchers found that the bacteria mix E. coli LPS which is common in intestinal bacteria with fibrinogen, and such small clot protein would form grumous fibrinogen bracket. LPS changes fibrinogen to make it form abnormal clots that are similar to the clots causing heart disease, stroke and the formation of deep vein thrombosis.

Researchers believe that LPS makes fibrinogen, and this deformation will spread in the protein. This is very similar to the way of prion protein deformation which causes BSE (bovine spongiform encephalopathy). Since LPS can induce inflammation, so it will increase the blood levels of fibrinogen, thus further increasing the risk of diseases associated with blood clots. Overactive blood clotting is also the characteristics of rheumatoid arthritis and Alzheimer's disease. These diseases are related to high iron content. Our body generally maintains the iron content in the blood at a low level so that bacteria are dormant, thus inhibiting their growth.

They observed that LPS causes the formation of fibrin mat and it will bind to many other proteins. So this means that in other inflammatory diseases, it is related to the formation of amyloid protein mat, such as the condition occurs in the brains of patients with Alzheimer disease and Parkinson's disease. Earlier this year, other researchers found that after injecting bacteria to the brains of mice, amyloid plaques would form overnight.

What does it mean to these diseases on earth? Future research will find new ways to deal with these diseases, such as removing dormant bacteria in the blood and inhibiting inflammatory proteins they produce. Flarebio provides you with good-quality recombinant proteins like recombinant COLEC12.

HRG replacement therapy may provide a new strategy for the treatment of sepsis

When suffering from sepsis, controlling the shape and activity of key proteins of a group of white blood cells and raising the levels can improve the chance of survival and recovery, according some studies using recombinant proteins. Blood poisoning after injury or infection is called sepsis, and it is a major reason of death worldwide. When suffering from sepsis, the body's immune system would over operate, leading to blood insufficiency of its own tissues and organs and thus causing damages. However, the exact molecular mechanisms of sepsis and its processes are unclear.

Now, Professor Masahiro Horie West in Japan and his colleagues from Okayama University, Shujitsu University and Kinki University have shown that a natural protein called histidine-rich glycoprotein (HRG) plays a significant role in the prevention of sepsis. They found that HRG controls the shape and activities of leukocyte which is called neutrophil to make them flow freely and show right response in the fight against sepsis.

Nishibori team intended to verify the role of HRG, because when sepsis happens, HRG levels in patients drop dramatically. HRG protein is produced and secreted by the liver. It is known that HRG is involved in regulating the immune response as well as the promotion of antibacterial and antifungal activity. The research team induced sepsis in a group of mice and took the healthy group as a control group. They purified human plasma HRG and made use of a dose of HRG protein to treat certain sepsis mice.

The researchers found that mice given HRG rapidly showed spontaneous activity and began to recover from sepsis. Further investigation showed that inflammation of the lungs of the treated mice was much less than the untreated mice. The shape of neutrophils of mice given HRG was more rounded and spherical, which made them more freely to go through micro-capillaries and veins. While the neutrophils of sepsis mice showed irregular cell shapes. This in turn triggers unwanted activity, because metamorphotic neutrophil will attach to other cells and establish cell mass, restricting blood flow.

"The reduce of plasma HRG is a fundamental way of incidence of sepsis," the authors stated in their paper published in the journal eBioMedicine (2016) , "HRG replacement therapy may provide a new strategy for the treatment of sepsis."

Further research is needed in healthy subjects and patients with sepsis, upstream signaling processes involved in HRG action. Further research will also determine whether HRG dose may be a valuable method for the treatment of patients with sepsis. Flarebio provides you with high-quality recombinant proteins such as recombinant CDH4 at reasonable prices.

New hope for developing new breast cancer drugs

Australian National University announced on 10th that researchers of the school have new findings of a group of proteins which helps to turn on or off some gene expression in the blood cell generation process, which helps to develop new and more effective breast cancer drugs.

Through a lot of studies using recombinant proteins such as recombinant horse proteins, researchers reveal the working mechanism of a group of specific proteins - chromatin helicase DNA binding protein (CHD). The group of proteins consists of the nucleosome remodeling deacetylase. This enzyme can turn on or off certain gene expression in the replication process of blood cells and stem cells. One of the proteins, CHD4, is associated with breast cancer, while there are no drugs specifically for this protein among existing drugs to treat breast cancer.

Dr. Daniel Ryan from Medical Research Centre of John Curtin at the Australian National University said that some currently-used breast cancer treatments are effective, but their mechanisms are not clear. While the research he is undertaking reveals the working mechanism of CHD4, which would make it possible to specifically develop super drugs of this protein for the treatment of breast cancer later. More precisely targeted therapies will reduce the toxicity of the drug and reduce resistance.

He said the researchers still need to break down this enzyme in order to explore how different proteins work with each other and to learn how complex molecular structures operate. Flarebio Biotech LLC is a National High-Tech Enterprise with research, production and sales as one. It provides you with superior recombinant proteins like recombinant ITGB2 at good prices.

To synthesize new-type proteins using artificial genes

Synthorx, an emerging biotechnology company located in La Jolla of California, is designing a micro-organism which has six gene codes. The approach is to add artificial X and Y base to the original gene system composed of A, T, G, and C. These micro-organisms don't have same kinds in nature, and Synthorx uses them to design new proteins. According to research using recombinant mouse proteins, these proteins are expected to become the cornerstone of future painkillers, antibiotics and targeted cancer drugs.

Romesberg is one of the company founders. Two years ago, nobody made anything useful with new synthetic X and Y bases, but Romesberg made a goal of making use of conventional chemical methods to develop new drugs. This is obviously an extremely complex process.

The birth of X and Y is of course a milestone in the scientific community, but the real challenge of Synthorx is to use these codes to produce new proteins. Theoretically, by simply adding X and Y, number of amino acids for building proteins can be improved up to 172 kinds, but it is only 20 in the natural state. By adding the XY codes to DNA, the cells can use as many as 172 kinds of proteins to build amino acids, which is far more than the original 20 kinds.

By using artificial amino acids, that scientists can make the combination of existing proteins and their target substance stronger so that the effect of drugs can be more potent. Another idea is to enhance the specific combination of proteins and their target substance through artificial amino acids in order to avoid the side effects of protein binding to non-binding target materials.

Currently, a project of Synthorx is dedicated to turn the venom of a kind of spider into a non-opioid and non-addictive painkiller. The CEO of Synthorx Court Turner said, "Although E. coli also can produce insulin, the only way so far for us to obtain extra insulin is to take injections every day."

Adding artificial amino acids to the insulin molecule can make it more durable. Thus, diabetes patients only need insulin injections every few days. There is no doubt that if this technology can be achieved, it will be a revolution. But it is still too early to dream for the wide use of artificial genes. Although artificial genes can produce amino acids, currently we don't have the ability to make proteins with synthetic amino acids. Flarebio offers recombinant proteins of good quality such as recombinant App.

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.

Get to know spontaneous autoimmune diseases better

A group of scientists led by researchers at Stony Brook University conducted experiments using recombinant human proteins and discovered a new mechanism of a bacterial toxin inhibiting inflammation. Their research showed that a toxin in Yersinia - bacteria agent of plague, can target inhibits protein pyrin. Hereditary autoinflammatory disease - Familial Mediterranean Fever (FMF) - is induced by sustained activation of pyrin protein which is caused by gene mutation.

The study was published in the journal Host Cells and Microorganisms, and it can be used to better understand the genetic origins of FMF and to explore new therapies for the treatment of these diseases.

"This finding is very significant because the popularity of Mediterranean-origin people suffering from Familial Mediterranean Fever (FMF) is very high, and the findings may explain the natural selection process behind the disease," Dr. James Bliska from Molecular, genetics and microbiology department of Stony Brook University School of Medicine, the lead author and professor said, "In addition, bacterial toxins would hijack the body kinase and phosphorylate and inhibit pyrin protein. This process can be converted into the process of treatment of FMF."

Hereditary inflammatory diseases brought by FMF usually occur at some time in childhood and would persist throughout adulthood. There are treatments, but no cure. For example, complications such as arthritis and vasculitis can appear long after the onset of inflammation. Thousands of people from different ethnic origins of the Mediterranean, such as Armenians, Italians, Greeks and Arabs, are suffering from FMF. Flarebio provides you with good-quality recombinant proteins such as recombinant ACSL3.

The protein the anti-diabetic drug Metformin specifically acts on

An international research team Nagoya University consists of several institutions recently announced that they successfully discovered which protein the anti-diabetic drug Metformin specifically acts on. This is the first time that scientists prove drug effects from the cellular level, and related results have been published in well-known American science journal. The experts say they got the results using recombinant rat proteins that Metformin will strengthen the intracellular material transfer weakened by diabetes through NHE proteins.

Metformin mainly acts on human liver and muscles. Although the drug has been demonstrated to have the effect of reducing blood glucose level, the scientists have been unable to ascertain which protein it acts on in cells.

The research team led by distinguished Professor You Young Jai at Nagoya University confirmed that metformin would act on a protein called NHE. NHE protein acts as a porter which intakes and egresses substance in and out of cells. By controlling pH, the speed of transporting materials can be finely adjusted.

Professor You Young Jai said that Metformin will strengthen the intracellular material transfer weakened by diabetes through NHE proteins.

The researchers used C. elegans to conduct related experiments. When investigating genetic mutation in C. elegans, they found that the C. elegans of NHE proteins can't be produced, and metformin had no effect on it. For Drosophila which is impossible to produce NHE proteins using recombinant DNA technology, metformin was also not effective. Related studies confirm that metformin treats diabetes by acting on NHE proteins. Flarebio offers recombinant proteins of good quality such as recombinant colec12 at great prices.

What is the disease that kills millions of American starfish?

Recently a large number of American starfish are found dead caused by strange diseases. There is no exaggerated that it may be called catastrophic. The researchers used recombinant proteins to conduct the research.

"It's staggering, really, the millions of stars that have died. It is not apocalyptic or extreme to say that," says Drew Harvell, a biologist at Cornell University, describing what is widely regarded as one of the worst marine disease events ever recorded.

The starfish is also called sea stars. Millions of the starfish died in recent years. They had their legs curl up and pull away from their bodies, breaking the animals to pieces before they turn to mush, often in a matter of days. Scientists are struggling to find out the reason. Once densely packed onto the rocks and on the ocean floor, the key predators are simply missing from some locations, their numbers cut by 95 percent or more.

As early as in 2013, this phenomenon called Sea Star Wasting Syndrome was noticed by rangers in Olympic National Park in Washington state. It has now been documented from California to Alaska, and led to die-off that is bigger and more widely spread than any seen before.

There was a group of researchers published their findings indicating strong evidence that a virus was causing the disease last year. Now researchers are studying why the so much more widespread and deadly. They are considering how warmer water brought by climate change is affecting the virus, starfish and the ecosystem. "We've had anomalously warm oceans for the last two years. Really, what we would call hot water. It is really the dominant thing to consider," Harvell said.

The problem is urgent to be solved even through it's hard to collect data on a big scale. The sea star is kind of the mascot of the intertidal. We should protect these sea stars, the ocean, the ecosystem, thus protecting ourselves. Flarebio provides recombinant proteins of high quality such as recombinant app.

AG1 gene is essential for rice seeds to live in water

A gene was identified to help rice seeds to survive when grown underwater. The study was published in the leading scientific journal Nature Plants by A team of scientists from the University of California, Riverside and the International Rice Research Institute (IRRI), the Philippines. The study using recombinant proteins such as recombinant rat proteins shows that the gene controls the availability of sugar to a growing seed shoot—especially when under flooded conditions.

"The seed of rice is unusual among crops because it can germinate and grow into a young plant that can capture light energy even when the entire process occurs underwater," said Julia Bailey-Serres, one of the paper's authors and a professor of genetics at UC Riverside. "The gene identified—the AG1 gene—helps in this process by allowing energy reserves that are in the seed to be efficiently moved to the growing shoot. The seed planted underwater grows into a seedling that can escape a shallow flood."

There was a gene called SUB1A discovered previously to enable rice plants to survive complete submergence due to a seasonable flood. But this new gene is opposite of that. Bailey-Serres says that Plants with SUB1A essentially hibernate when they are underwater; a situation where energy reserves are safeguarded.

AG1 creates an 'all or nothing' escape mechanism that tricks the seed into thinking that more sugar should be given to its shoot—the plant part that grows into stems and leaves—so that the seed underwater is able to more quickly grow and reach the surface of the water. The mechanism can work up to a water depth of 10 cm and can get 'activated' as soon as the seed is sown underwater.

This gene is one of a family of 13 genes in rice. Other family members are shown to help to move suger from leaves to the young developing seed in fertilized flowers. The important gene is supposed to tell the cell that it does not have enough sugar—keeping the tap open for more to be moved from the seed to the growing shoot.

AG1 works well on moderate stress conditions. When we combined it with the SUB1A gene in the same genetic backgrounds it worked well, although they have opposing mechanisms. However, in some severe stress conditions, AG1 alone is not sufficient. It needs some additional quantitative trait loci (QTLs) or genes that complement the AG1 mechanism.

There is another question they are faced with - Whether seed can be directly seeded underwater – requiring the escape strategy – can also carry the SUB1A gene for submergence tolerance. There are more to be investigated to find the answer. Flarebio offers recombinant proteins such as recombinant INSRR at competitive prices.

The mechanism of gene defect causing to autism in mice experiments

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

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

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

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

A financing of 47 million of dollars to develop therapy for Alzheimer's disease

Proclara Biosciences is a biotechnology company focused on developing new treatments for protein misfolding diseases and seeking for strategies which can redress the neurodegenerative disease molecules of β-amyloid, tau and α-synuclein. Recently, Proclara Biosciences conducted research using recombinant human proteins and announced the completion of $ 47 million E round of financing. At the same time, the focus product candidate NPT088 of the company for the treatment of Alzheimer's disease enters 1B clinical trials.

The financing in this round is led and invested by private investors and Merieux Developpement. The funds will be used to develop product candidates of Alzheimer's disease, Parkinson's disease and other diseases, to support further clinical studies of NPT088 as well as to promote the study of the latency molecules. So far, Proclara Biosciences has a total financing of $ 101.8 million.

Proclara Biosciences was formerly known as Neuro Phage Pharmaceuticals. CEO Franz Dr. Hefti said the name change is an important milestone, marking that the company will move towards the direction of finding new treatments of weak protein misfolding diseases to address the urgent needs of the majority of patients.

Proclara provides transformational therapy for Alzheimer's disease and other neurodegenerative diseases. The survey found that most studies of the neurodegenerative diseases only aims for one type of misfolded proteins, while Comprehensive amyloid protein interaction motif owned by Proclara can simultaneously monitor multiple misfolded proteins. NPT088 is the key project of Proclara Bioscience Company. It acts on two protein aggregates which affect Alzheimer's disease: amyloid β (Aβ) and tau protein. It is the most suitable method for treating complex diseases. Flarebio offers recombinant proteins such recombinant Cdh10 at competitive prices.

Scientists have identified a gene that can keep crops healthy under adverse condition

As you know that plants rely on structures called chloroplasts within their cells to carry out photosynthesis—the process used to capture energy from sunlight by converting carbon dioxide from the air into sugars. During times of stress such as drought, though, the same reaction can also generate substances known as reactive oxygen species, which are toxic to plants and cause them to become damaged or even die. The research used a lot of recombinant proteins like recombinant horse proteins.

With the population growth, increasingly shortage of natural resources and the treat of climate change, to develop crops that can survive sub-optimal growing conditions seems Researchers from Oxford University has found a gene that helps plants to remain healthy during times of stress.

According to Professor Paul Jarvis, from the Oxford University's Department of Plant Sciences, the development of chloroplasts is controlled by the presence of a gene known as SP1, which governs the passage of the proteins involved in photosynthesis through the chloroplast's outer membrane. It is suspected that the gene might use this ability to help plants survive in hostile conditions.

The researcher team led by Professor Jarvis wanted to find out if SP1 helped plants to remain healthy by limiting the production of the toxic compounds made during photosynthesis in harsh conditions and has carried out experiments to investigate the idea. Theyworked with three versions of a cress plant known as Arabidopsis thaliana: the naturally occurring wild type, a mutant plant lacking SP1, and an engineered plant that over-expressed SP1. The results indicated that SP1 was responsible for the resilience.

Another set of experiments was carried out to establish how SP1 works at a molecular level. The results demonstrated that SP1 reduces the production of toxic compounds by limiting photosynthesis in times of stress, making plants less likely to suffer serious or fatal damage.

"All plants have the SP1 gene,' explains Professor Jarvis." Now it's just a question of getting plants to over-express it so that they can survive in adverse conditions.'

The researchers are working with more plants to see whether the findings can be used in a wider variety of plants. Hope that the SP1 technology can benefit the improvement of the crop output all around the world. Flarebio offers recombinant proteins such as recombinant Cdh5 at good prices.

Biological engineers use customized protein-based sensor to detect viral infection

Biological engineers from MIT have developed a modular system of proteins using recombinant mouse proteins, which can detect a particular DNA sequence in a cell and then give a response like cell death. According to the researchers, the system can be customized to detect any DNA sequence in a mammalian cell and kill cancer cells or cells infected with a virus.

"There is a range of applications for which this could be important," says James Collins, the Termeer Professor of Medical Engineering and Science in MIT's Department of Biological Engineering and Institute of Medical Engineering and Science (IMES). "This allows you to readily design constructs that enable a programmed cell to both detect DNA and act on that detection, with a report system and/or a respond system."

The technology is based on a type of DNA-binding proteins known as zinc fingers. These proteins can be designed to recognize any DNA sequence. "The technologies are out there to engineer proteins to bind to virtually any DNA sequence that you want," says Shimyn Slomovic, an IMES postdoc and the paper's lead author. "This is used in many ways, but not so much for detection. We felt that there was a lot of potential in harnessing this designable DNA-binding technology for detection."

The researchers needed to link zinc fingers's DNA-binding capability with a consequence-either turning on a fluorescent protein to reveal that the target DNA is present or generating another type of action inside the cell. To create the new system, they exploited a type of protein known as an "intein" and split it into two pieces. The split protein pieces are called "exteins". They only become functional once the intein removes itself while rejoining the two halves.

They decided to divide an intein in two and then attach each portion to a split extein half and a zinc finger protein. The zinc finger proteins are engineered to recognize adjacent DNA sequences within the targeted gene, so if they both find their sequences, the inteins line up and are then cut out, allowing the extein halves to rejoin and form a functional protein. The extein protein is a transcription factor designed to turn on any gene the researchers want.

The researchers also deployed this system to kill cells by linking detection of the DNA target to production of an enzyme called NTR. This enzyme activates a harmless drug precursor called CB 1954, which the researchers added to the petri dish where the cells were growing. When activated by NTR, CB 1954 kills the cells.

There will be more versions in the future which bind to DNA sequences found in cancerous genes and then produce transcription factors that would activate the cells' own programmed cell death pathways. This protein-based sensor can be of great significance. Flarebio provides recombinant proteins such as recombinant CDH11 at competitive prices.

The action mechanism of Alzheimer's disease has been revealed

Alzheimer's is the most common form of dementia globally and affects so many people in the world. It is the fourth leading cause of death in individuals over the age of 65. It is the only cause of death among the top ten that cannot be prevented, cured or even slowed down. A lot of research using recombinant mouse proteins have been conducted to study the disease.

However, there is good news. Scientists at Trinity College Dublin have figured out a fundamental mechanism underlying the development of Alzheimer's disease. It may lead to new forms of therapy for those living with the condition.

Alzheimer's disease is characterized, in part, by the build-up of a small protein ('amyloid-beta') in the brains of patients. Impaired clearance of this protein appears to be a major factor in the build-up of plaques, and then in the disease process itself. While the mode by which amyloid-beta is cleared remains unclear, it is evident that it needs to be removed from the brain via the bloodstream.

Those in the brain have properties that strictly regulate what gets in and out of the delicate tissue. It is what is known as the blood-brain barrier (BBB). The BBB functions as a tightly regulated site of energy and metabolite exchange between the brain tissue and the bloodstream.

The research shows that distinct components of these blood vessels termed tight junctions are altered in Alzheimer's disease. This alteration is thought to be an entrained mechanism to allow for the clearance of toxic amyloid-beta from the brain in those living with Alzheimer's disease. The research also highlights the importance of understanding diseases at the molecular level. The concept of periodic clearance of brain amyloid-beta across the BBB could hold tremendous potential for Alzheimer's patients in the future. What remains to be done is figure out how to achieve this. Flarebio provides superior recombinant proteins such as recombinant CDH4 at good prices.

Researchers unexpectedly find new vaccine which is effective to hepatitis B

A new anti-grass pollen allergy vaccine (BM32) also can be effective against hepatitis B virus infection. The study used a lot of recombinant proteins such as recombinant horse proteins and was conducted by the Institute of Physiology, Medical University of Vienna pathology experts, published in the journals EBioMedicine.

BM32 vaccine is developed based on innovative recombinant peptide - carrier technology. Compared with other immunotherapies, the technology shows fewer side effects on allergy sufferers. The technology was conducted under the dominant of Rudolf Valenta from Medical University of Vienna.

In a IIb Phase trial led by the research institution, Carolin Cornelius found that BM32 can also resist hepatitis B virus infection when it prevent grass pollen allergy at the same time. Cornelius said, "We can prove that for those people who weren’t vaccinated with hepatitis B vaccine previously, the effective resistance rate against hepatitis B virus would reach 80% after taking BM32 vaccine." Related researchers said that the concept of peptide - carrier fusion proteins perhaps would provide new ideas for the development of immunotherapy which can improve hepatitis B infection in the future.

Cornelius continued, "We are currently researching on whether the vaccine is able to specifically resist hepatitis B virus. Hepatitis B virus infection is very common nowadays. About 350 million people worldwide carry the hepatitis B virus in the blood. For people who have taken hepatitis B vaccine, there is also 5-10% of them may respond to the virus." Flarebio provides you with good-quality recombinant proteins like recombinant ITGB2.

Optimized gene therapy of Parkinson's disease shows great success

Levodopa is a commonly-used drug to alleviate the symptoms of Parkinson's disease. However, patients taking the drug mostly feel disappointed as the final outcome. When initially taking levodopa, the patient's symptoms in the tremor and balance would be mitigated and controlled. But as time goes on, the effect of drugs will become increasingly worse. They may have to use ultra-high doses of the drug, and some patients may spend several hours in a paralyzed state in almost every day.

Today, Voyager Therapeutics Company located in Cambridge, Massachusetts thought that gene therapy can prolong the efficacy of the drug levodopa. Currently, the company's gene therapy has entered clinical trials with the aid of recombinant proteins such as recombinant mouse proteins.

Parkinson's disease is due to the death of neuron which produces dopamine in brain, resulting in difficulties of patients in athletic ability. People plagued by this disease include the famous boxer Muhammad Ali and actor Michael Fox. Although the reason leading to the death of brain dopamine neuron is still not fully understood by scientists, the reason for the failure of the drug levodopa has been found. Levodopa is the precursor of dopamine. It can be turned into dopamine under the disposal of aromatic L- amino acid decarboxylase (AADC) in the brain. However, in the brain of patients with Parkinson's disease, with the passage of time, AADC levels are decreasing. This results the condition that L-dopa can't be sufficiently converted to dopamine.

The strategy of Voyager wishes to inject adeno-associated virus (AAV) which expresses AADC into the patient's brain through gene therapy, thereby restoring AADC levels in the brains of patients and prolonging the efficacy of levodopa. "We have spent 60 years to study the pharmacology of dopamine," said Steven Paul, CEO of Voyager. "If we can put genes into the right brain tissues at the right time, then there is no reason that we don't succeed."

However, to put the correct gene into the right brain tissue to ensure a sufficient number of expressions is not an easy task. In order to ensure that AADC can express in the correct tissue, Voyager specially designed an injection system which can put the virus carrying AADC gene into the brain. In recent clinical trials, the patients will lie on the MRI machine to accept injection of the virus. Thus, brain surgeon can see the position of the putamen in the brain, thus ensuring the injected virus can cover this important area which needs AADC protein expression. Meanwhile, Voyager Company adds a chemical marker on AADC protein so that the doctor can see the position of proteins which express in the brain after surgery. In ongoing clinical trials, the gene therapy of Voyager has shown a significant effect on some patients.

Dr. Krystof Bankiewicz, one of the co-founders of Voyager said, "We think the failure of previous gene therapy of Parkinson's disease is that the method of gene transfer has not been optimized." Whether the optimized gene therapy of Voyager Company would succeed? We look forward to seeing the results of their clinical trials. Flatebio offers recombinant proteins of good quality like recombinant Cdh4 at competitive prices.

New hope for patients with Alzheimer's disease

A new therapy of Alzheimer's disease brings new hope for people to cure this incurable disease. This therapy seems to be able to reduce the major pathogenic factor protein deposits in the brains of patients. According to research published by American and Swiss researchers in the journal Nature, the researchers used recombinant human proteins to conduct research and found that the new treatment also slows down the decline of brain processes.

The researchers divided 165 patients with Alzheimer's disease into two groups to conduct research. A group of patients took placebo, and the other group took Aducanumab antibody once a month. Such antibodies can reduce the typical protein deposits in brains of patients with Alzheimer's disease. Before typical features of Alzheimer's disease such as memory loss, thought and language barriers occur, the brains of patients have deposited amyloid plaques. We can call them β-amyloid plaques.

After a year of observation, a group of patients showed significant reduce of protein deposits. Moreover, the decline rate of cognitive function in patients was significantly slower than patients who took placebo. But the researchers believed that the positive role of the new antibody on cognitive function needs further investigation. However, scientists' findings confirm the hypothesis of amyloid protein and correctness of continuing to study the antibody which treats Alzheimer's disease.

Alzheimer's disease specialist Christian Haass at Neurodegenerative Disease Center Germany (DZNE) said previous studies also found the possibility of removing brain protein deposits, but it can't restore lost memories or stable memory. In contrast, the biggest difference in this research result is that we can confirm that reducing the protein deposits and memory stability is closely related. This is of course the main goal we want to achieve.

Haas said that this is undoubtly a very great progress that has been ever made in this area. Because the results of this study clearly indicate that antibody therapy is effective for the treatment of Alzheimer's disease. Antibody therapy can maintain memory. Haas believes, however, it is too early to refer it as "breakthrough". This is a small-scale test, but it is definitely the first to have some positive impacts on the memory of Alzheimer's patients at least.

Previous multiple tests showed that Alzheimer's disease has already develops long before memory loss, because protein deposits have been formed at an earlier time. Patients must be treated early if they want to prevent progression of the disease. It will be too late for most patients if they go to the doctor when the memory is fading. Flarebio provides you with good-quality recombinant proteins such as recombinant ITGB2 at good prices.

A mechanism is found to slow down brain stem cell aging

Recently scientists from the University of Zurich have identified a novel mechanism of how neural stem cells stay relatively free of aging-induced damage. A diffusion barrier regulates the sorting of damaged proteins during cell division. As we know that neural stem cells generate new neurons throughout life in the mammalian brain. But after researching with recombinant dog proteins, they knew that the potential for regeneration in the brain dramatically declines with age. The mechanism just found is of great significance.

Yeast is useful for making wine, bread and brewing beer. At the same time, they are also a good model for neural stem cells in the mammalian brain. It was known that with every division cellular aging factors are asymmetrically distributed between the mother and the daughter cell, allowing for rejuvenation and full life span of the daughter independent of the age of the mother cell. The presence of a diffusion barrier that restricts movement of molecules from one side to the other side of the cell during cell division is partially responsible for that.

To dispose age, Sebastian Jessberger of the Brain Research Institute led a group of scientists to conduct a research and the results showed that also the stem cells of the adult mouse brain asymmetrically segregate aging factors between the mother and the daughter cells. It is a diffusion barrier in the endoplasmic reticulum that is responsible. The barrier keeps the stem cells relatively clean by preventing retention of damaged proteins in the stem cell daughter cell.

Scientists found that the strength of the barrier weakens with advancing age. The weakening leads to reduced asymmetry of damaged protein segregation with increasing age of the stem cell. This is supposed to be a mechanism related to the reduced regeneration capacity in the aged brain for stem cells that retain larger amounts of damaged proteins require longer for the next cell division.

The discovery of the new mechanism is an exciting thing. It is our first step to understand the molecular constituents and the worth of the barrier for stem cell division in the brain. And what remains to be explored is whether the barrier is established in all somatic stem cells of the body. The answer may help finding new way of target age-dependent alterations of stem cell activity in human disease. Flarebio provides superior recombinant proteins like recombinant Pigr at good prices.

Scientists discover that a single gene mutation can change entire biological communities

New research through recombinant rat proteins has found that one gene mutation in a single species can trigger great changes in whole biological communities.

Scientists from Trinity College Dublin use bacteria to replicate ecological systems in the lab and found that mutations of a single gene that change how one bacterial species interacts with others had huge structural impacts across their multi-species microbial communities. These mutants produce biofilms according to their ability and many of which cause great health problems in body. It had chain effect on other species and completely changes the structure of the communities.

"We know that predators are hugely important in influencing how ecosystems are structured, as they control the numbers and diversity of other species in the food web. It is incredible that such a small genetic change can cause these mutants to completely alter communities as much as the extinction of something as important as a predator," said Assistant Professor in Zoology at Trinity, Dr Ian Donohue.

The study shows wide scope for fine-scale genetic differences within populations to change entire ecosystems including microbial ones to lakes, forests and marine system.

"It's amazing to know that just one change in a single gene has the potential to have such a huge effect that it can change whole ecosystems," said Deirdre McClean, lead author of the study and PhD Researcher in Zoology at Trinity.

The results will be helpful to disease researchers, drug developers, ecologists and even geneticists. Besides, better understanding of the effect will be critical to develop treatments aimed at manipulating our gut microbiota specifically. Flarebio provides recombinant proteins of good quality like recombinant APP at good prices.

Scientists develop new technology to repair broken proteins

A new technology is developed to help scientists understand the work process of proteins and fix the broken proteins. Researchers used to make use of many kinds of recombinant proteins such as recombinant mouse proteins and recombinant dog proteins to conduct related research. The user-friendly technology is believed to lend a hand to finding new drugs for many diseases, including cancer.

As we know that the human body has a coordinating way of turning its proteins on and off to alter their function and activity in cells. It is phosphorylation, which is the reversible attachment of phosphate groups to proteins. They provide an enormous variety of function and are essential to all forms of life. However, we know little about the detail of this dynamic process.

Researchers have built a cell-free protein synthesis platform technology that can manufacture large quantities of these human phosphoproteins for scientific study using a special strain of E. coli bacteria. The technology can enable scientists to learn more about the function and structure of phosphoproteins and identify the one which are involved in disease. The study was published Sept. 9 by the journal Nature Communications.

Trouble in the phosphorylation process is a trait of disease like cancer, inflammation and Alzheimer's disease. The human proteome is estimated to be phosphorylated at more than 100,000 unique sites. It makes study of phosphorylated proteins and their role in disease is a tough task.

The new technology just developed begins to make the job a tractable problem. It can make these special proteins at unprecedented yields, with a freedom of design that is not possible in living organisms. The consequence of this innovative strategy is enormous in the long run.

Michael C. Jewett is a biochemical engineer who led the Northwestern team. He uses cell-free systems to create new therapies, chemicals and novel materials to impact public health and the environment. Jewett and his colleagues combined state-of-the-art genome engineering tools and engineered biological "parts" into a "plug-and-play" protein expression platform that is cell-free. Cell-free systems activate complex biological systems without using living intact cells. Crude cell lysates, or extracts, are employed instead.

To be specific, the researchers prepared cell lysates of genomically recoded bacteria that incorporate amino acids not found in nature. This allowed them to harness the cell's engineered machinery and turn it into a factory, capable of on-demand biomanufacturing new classes of proteins.

The manufacturing technology will help scientists to unlock the phosphorylation 'code' that exists in the human proteome. The study was published on Sept. 9 by the journal Nature Communications. Flarebio provides you with superior recombinant proteins like recombinant Adam19 at good prices.

Fluorescent protein helps to conduct the study of arrhythmia

Stem cell-derived cell models play an increasingly important role in cardiac dysfunction studies. Researchers at Technical University of Munich (TUM) have successfully produced cells which are helpful to the studies of cardiac cell characteristics. Using glowing molecular sensors and recombinant human proteins will not only make the electrical activity of the cells visible, but also makes it possible to quickly identify the type of cell for the first time.

In the past decade, it has been possible to produce so-called induced pluripotent stem cells in the laboratory. These stem cells are derived from white blood cells - for example - they can be infinitely replicated in the laboratory and turn into all possible cell types. For example, heart cells generated in this way can be used to investigate arrhythmia. The can be used in animal experiments in the application and can't easily remove samples of tissue from the patient's heart. However, the cultured heart cells provide an opportunity to study such diseases in an approach of "microcosm".

"Our study addresses several problems using this type of cell model", said Dr. Daniel Sinnecker of Heart disease at Technical University of Munich. Heart cells produced in laboratory still have the problem of how to best measure the electrical activity. In the past, microelectrode is the most commonly to be used to directly determine the electrical signal of cells. However, this process is quite complicated and can only be used on a small number of cells.

The article published by Daniel Sinnecker and his team in the journal the heart of Europe offers a possible solution for the problem. Unlike making cell attaching microelectrode and other methods, the scientists used a biosensor. These are derived from fluorescence, i.e. Luminous - deep-sea jellyfish protein. Introduce DNA containing these sensor proteins "construction plans" into heart cells and then the protein of the sensor is produced. If giving labeled heart cells with a specific wavelength of light stimulation, they will produce light at different wavelengths. The returned exact color of the light depends on the voltage difference between the inside and outside of cells. Therefore, scientists can use a special camera to measure and record action potentials of single cells.

A special feature of this new approach is that the inserted DNA can be coupled with specific recognition sequences which are so-called promoters. These sensors ensured that the presence of protein production is only in a specific type of heart muscle cells. So it can capture the electrical signals from cells of atrium, ventricles and atrionector. Flarebio offers recombinant proteins of good quality such as recombinant Ext2 at competitive prices.

A small molecule that can help to reduce AML relapse

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

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

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

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

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

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

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

Human body will pay more for anti-infection

Evidence from the study of a research team led by Tobias Lenz and Shamil Sunyaev conducted researcher using recombinant mouse proteins and found that the variations of deleterious gene may be the cost of our genetic diversity pays in other ways which are advantageous to us. They analyzed a group of immune system proteins to help to detect foreign molecules. These genes of these proteins contain many variation points. This diversity ensures our immune system to recognize a wide range of pathogens.

The selective special form retains this change of immune proteins within a group: scientists describe it as balancing selection. The results it produces is that when a gene of several alternative variants conferred a survival advantage, it will not be selected to eliminate.

Scientists suspect that balancing selection can sometimes lead to protection against harmful gene variants. They used the example of immune system genes to conduct computer simulation of different types of choices. In these tests, they found that balancing selection not only increases the diversity of immune proteins, but also affects the adjacent DNA fragments. At the same time, reducing the total number of variable sites increases the frequency of these variants in the population - even if they are harmful.

They then compared simulation results and the genetic analysis data of 6,500 people. The analysis confirmed their suspicions. Harmful genes can escape natural selection. "I did not expect that higher pathogen resistance may lead to some accumulation of deleterious mutations, but this mutation in the crowd sustained level surprised me. It will be interesting that the number of human genetic diseases can be traced back to the pathogen we are exposed to in the development process, "Tobias said.

Next, the researchers want to check out whether the balancing selection of other sites in the genome is associated with the frequent occurance of harmful genes in the populations. Flarebio offers recombinant proteins of good quality such as recombinant Cdh10 at competitive prices.

Protein makes sense in a cell

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

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

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

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

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

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

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

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

New mechanism of brain disease helps to develop new therapy

A new study published by Hong Kong University of Science and Technology discovered the a new mechanism which causes autism, mental retardation, schizophrenia and other mental disorders, which is helpful for the development of new therapies for these diseases in the future.

A research team led by Professor Zhang Mingjie at Life Sciences of HKUST used recombinant human proteins and found that the human brain is responsible two molecules SynGAP and PSD-95 which are the main components of proteins in "postsynaptic density area" where nerve signals are received. It can be assembled into a network structure, and this structure will form a stable "oil-droplet shape" droplets.

The study also found that defective proteins in the brain of the autism patients would change the composition of "oil-droplet shape" droplets, thereby changing synaptic signaling activity. The researchers said these findings could explain the etiology of autism and help to understand why gene mutations altering the interaction among these proteins will lead to a series of central nervous system diseases which haven't got a method of treatment, thus injecting new inspiration for the development of therapies.

It is understood that other neuropsychiatric disorders include schizophrenia, mental disorders, depression and so on, and they have the same formation mechanism. The research results have been published in the August 25 issue of the scientific journal Cell. Flarebio offers recombinant proteins such as recombinant Cdh10 at competitive prices.