Understanding more about the dinoflagellate's mystical genome

Dinoflagellates usually have a good life when in good times. They live free-floating in the ocean or symbiotically with corals, or as lunch to a host of mollusks, tiny fish and coral species. Some of them make glowing waves at night since they are bioluminescent. However, things will get worse when conditions are wrong. Dinoflagellates poison shellfish beds with red tides and abandon coral reefs to a slow, bleached death.

This happens more and more frequent. In order to find out the answer, UConn marine ecologist Senjie Lin led his research team and sequence the complete genome of dinoflagellate species S. kawagutii, becoming the first one who had done so. The results can be found in journal Science which also publishes other studies on recombinant human proteins.

The species of S. kawagutii is an important endosymbiont of coral reefs, providing them with sugars and nutritious compounds. When it is not present, the corals bleach white, cannot grow and tend to die. However, although metabolic wastes from the coral host provide an enriched supply of nutrients in the otherwise nutrient-poor oceanic habitat, the relation seems to be not enssential S. kawagutii. The researchers guess that when the dinoflagellates don't like the conditions, they can jump ship and turn themselves into impervious little cysts and wait for the right time to ecolonize corals. This performance also can explain that S. kawagutii has an awfully large genome for a symbiont. Usually endosymbionts and parasites depend on the cellular machinery of their hosts and lack many genes that free-living organisms have. So here comes the question: Why does S. kawagutii have so many? No one can explain now.

After analyzing the entire genome of S. kawagutii and comparing it with the genetic codes of related organisms which can be better understood, the team found some surprising things. For instance, they found genes associated with sexual reproduction. S. kawagutii typically reproduces asexually as other dinoflagellates do. A single dinoflagellate will simply split in two. However, when the dinoflagellates turn into cysts, they would reproduce sexually first, which mixes their genetic material with others, maybe in the hope that some of the offspring will gain traits better suited to the stressful environment. But sex related genes have never been found in other dinoflagellates. The results of the study show that K. kawagutii actually has had the bad times in corals.

They also found that S. kawagutii has a gene regulatory system that looks like it could regulate certain genes in corals. That's to say, the dinoflagellates may be manipulating their host's genetic expression in order to make the conditions more comfier for them.

Understanding the S. kawagutii's genome can help researchers better study other dinoflagellates which act many different roles in the ocean ecosystem, thus explaining how the environment changes affecting their way of life. Flarebio offers high-quality recombinant proteins such as recombinant APP at competitive prices.

New technology can track antitumor immune cells

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

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

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

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

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

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

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

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

Only particular animal species are infected by Salmonella

According to studies on recombinant human proteins, you may know that many strains of Salmonella bacteria are specific to certain species of animals. Some of them may infect cows, pigs, chickens or sheep, still others infect primarily humans.

Recently, a study by a team of scientists from University of Pennsylvania showing that slight variations in the coding sequence of proteins that bind Salmonella to host cells can determine what type of animal a particular strain infects. The findings were gotten using genomic techniques.

The team first focused on the analyses of Salmonella enterica serovar Typhimurium, a leading cause of food poisoning. But it is still a mystery for which the molecular basis for host preferences is.

Single nucleotide polymorphisms (SNPs), variations in the nucleotide sequence of DNA, were identified through the genomic analyses. They found a relatively large number of SNPs, in genes coding for Salmonella surface proteins or secreted factors.

Different host species would share patterns of these so-called non-synonymous SNPs, creating different protein sequences and structures.

Through analyzing of 15 genes in 580 strains of Typhimurium, the team found a high degree of variation and evidence of positive selection and strong evidence that the variation was associated with the particular strains' host specificity.

Further research will be conducted to determine the genetic differences that may separate a strain of Salmonella that causes a brief gastrointestinal illness from one that cause a major systemic disease.

The study was published in the Nature Communications. By the way, Flarebio offers superior recombinant proteins including recombinant Aoc3.

Squalamine can improve the treatment of Parkinson's disease

Scientists report that a compound which occurrs naturally blocks the molecular processes of Parkinson's disease and inhibits its toxic products. The study was completed using recombinant rat proteins by the University of Cambridge and the United States National Institutes of Health and other academic centers in Europe and America.

In the new study, the researchers conducted a series of experiments on the interaction between squalamine, α-synuclein and lipid vesicles. They found that squalamine inhibits protein aggregation by competing for binding sites on the surface of vesicles. By displacing the protein in this manner, it significantly reduces the rate of toxic particle formation. Further tests conducted in human nerve cells show that squalamine inhibits the toxicity of these particles.

Finally, the team tested the effect of squalamine in animal models of Parkinson's disease and used nematodes to express the α-synuclein gene in muscle cells. When the nematode develops, the α-synuclein gene prevents them from moving and the ingestion of salicylamine from the mouth can prevent such paralysis. All the results show that squalamine can be used as a basis for at least some of the symptoms of Parkinson's disease. Researchers said they are planning to conduct clinical trials on Parkinson's patients in the United States.

However, there are further studies to be confirmed, such as the exact benefits of squalamine and drugs may lead to any results. In particular, it is unclear whether squalamine can reach the brain-specific regions of the major molecular processes responsible for Parkinson's disease.

The researchers believe that the initiation of the investigation of salmianol to relieve other symptoms of the effect will be very interesting. By targeting the gastrointestinal system and influencing α-synuclein in the gut, the compound may alleviate severe constipation experienced by the patient. So this treatment can lead to other parts of the body cascade signal, at least in the peripheral nervous system relieve Parkinson's disease. Parkinson's disease has many symptoms. The researchers hope that this compound or its derivatives have a similar mechanism of action to alleviate some of these symptoms and to improve the patient's life at least. Flarebio offers high-quality recombinant proteins like recombinant TLR2 at good prices.

The gene Gpr182 has been caught to treat gastrointestinal cancer

Recently, an article published in the journal Clinical Medicine states that scientists have finally seized the Gpr182. Over the years, Gpr182 is like a fugitive criminal, so scientists are helpless. Studies using recombinant dog proteins have shown that Gpr182 can open the door for the treatment of gastrointestinal cancers if a solution can be found.

"The good news is that this is a completely new field. It's especially tempting from a medical point of view, because they shed light on the new g-protein-coupled receptor, a class of cell membrane proteins that are well suited to drugs," the researchers say. 40% of the approved drug target at g protein-coupled receptor. Therefore, the discovery of this new receptor plays a huge role for the understanding of gastrointestinal biology and improves the treatment of colon cancer and other diseases. At present, gastrointestinal cancer is the second leading killer cancer in the United States.

After a series of trials, the researchers found that colorectal cancer patients with colorectal cancer had significantly lower Gpr182 expression compared with healthy colon tissue. Further analysis also suggested that Gpr182 expression reduced in breast cancer, lung cancer and other types of cancer.

At the same time, the results suggest that manipulation of Gpr182 expression or activation may provide a new approach for the treatment of cancer, particularly for the treatment of gastrointestinal cancers. Omera Pharmaceuticals claims to have developed a small molecule that intersects Gpr182 and can help speed drug development. Flarebio offers high-quality recombinant proteins like recombinant ITGB5 at competitive prices.

This gene can control 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 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 through recombinant rat proteins, 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. By the way, Flarebio provides you with superior recombinant proteins like recombinant ITGB5.

To better learn transcription factors through SMiLE-seq

EPFL scientists have developed a technique through recombinant rat proteins to make DNA-binding proteins faster, more accurate and more efficient. The results were published in the Jan. 16 issue of Nature-Methods.

The gene contains the DNA code used to produce all the proteins in the cell. To begin the process, the gene must first be transcribed from DNA into RNA. This requires a huge family of DNA-binding proteins called transcription factors, which are of great interest to biologists because of their importance in gene expression. However, due to their pure numbers, their ability to combine into pairs and the difficulty of studying their DNA binding properties in the lab, scientists have known little about transcription factors despite of much effort.

The Bart Deplancke lab at the EPLL Institute of Biotechnology has now invented a new technology called SMiLE-seq, which can greatly accelerate the process with a small amount of transcription factors. The technology uses microfluidics: the science of controlling minute liquids in the same tiny space. Microfluidics is fast becoming an outstanding area of ??EPFL, bringing together many different fields and disciplines.

SMiLE-seq works by adding a small amount of transcription factors (or factors when detecting heterodimers) in microfluidic devices that have microchannel-sized chips that allow liquid to flow therethrough. Once the transcription factor is attached to the surface of the chip, large libraries of random DNA are gently pumped into the chip and flow through them. This allows the transcription factor to recognize its corresponding DNA sequence. Thereafter, the transcription factor-DNA complex is physically captured by dropping the microfluidic control button, and the unbound DNA is simply washed off.

Next, the bound DNA is removed from the device and ready for sequencing to identify which portion is captured by the transcription factor. This information is input into specialized software that allows the researcher to determine the DNA binding properties of transcription factors or heterodimers. This, in turn, helps to better predict the in vivo DNA binding profile.

The use of microfluidics in SMiLE-seq offers three major advantages: First, it reduces the amount of transcription factor required for this type of experiment because it only requires their picogram. Second, it greatly accelerated the experimental process, from a few days to less than an hour. Finally, SMiLE-seq is not limited by the length of the DNA target sequence, nor is it biased towards a stronger affinity protein-DNA interaction. Flarebio provides you with high-quality recombinant proteins like recombinant NPP1 at competitive prices.

Reactive nerve cells have firstly been cultured!

The official website of University of Pennsylvania School of Medicine has just announcement on17th that research team from the hospital James Abbe for the first time used the surgical excision of the brain tissue in the laboratory to culture adult nerve cells and to identify five types of brain cells and each cell synthesis of proteins. The study using recombinant human proteins has been published in the issue of Cell Reports this week.

The brain tissue in this trial did not contain tumor cells from seven patients, including three patients with epilepsy who received temporal lobe surgery after temporal lobectomy and four patients with glioblastoma after surgery. The researchers from excised tissue was picked out without any tumor cells used in part. When these tissue samples were obtained, they were immediately treated with papain, a proteolytic enzyme, to produce active neurons. They analyzed more than 300 active cells one after the other and identified five known brain cell types: oligodendrocytes, microglia, neurons, endothelial cells and astrocytes.

Because it is not possible to study individual neuronal cells in adult patients, human brain disease awareness and development-related therapies have been slow. "It's amazing how we can nurture nerve cells, and we're finally going to have a mystery about the most mysterious organism in the body," says Abbein. "Previous studies of geriatrics rely primarily on animal models, but this time, Neurocytes originate in different age groups from the age of 20 to 60 years and can be used to detect the difference of molecular markers between the nerve cells of the elderly and the young people so as to provide a new research system of geriatric diseases."

The team used RNA sequencing to find more than 12,000 genes in these cells, and each has hundreds of different RNAs. They also identified long-chain non-coding RNAs corresponding to different cell types, resulting in a completely different gene expression in each patient's nerve cells, which provided strong support for personalized medicine. The researchers said that the new study on the use of cell replacement therapy to repair damaged brain tissue "repair neurosurgery" is of great significance. It is expected to make this therapy as soon as possible in human clinical trials. Flarebio offers high-quality recombinant proteins like recombinant Cdh11 for you research.

Scientists have found new drugs that can be used to prevent spread of breast tumor

A new study has found that drugs approved for the treatment of estrogen receptor-positive breast cancer have the potential to prevent the spread of refractory triple-negative breast cancer. The study using recombinant horse proteins and published in Nature Communications shows that the drug blocks triple-negative breast cancer in many models by blocking an enzyme pathway called CDK4 / 6 - the CDK4 / 6 inhibitor.

Estrogen Receptor Positive (ER Positive) Breast cancer is one of the most common forms of breast cancer, which contains estrogen receptors. When these receptors receive the hormone signal, it will promote cancer cell growth. Similarly, in progesterone receptor-positive (PR-positive) breast cancer, cancer cells containing progesterone receptors can promote cancer cell growth, whereas HER2-positive breast cancer cells on the HER2 gene receptor may exacerbate the condition. Fortunately, there are some hormones for the treatment of breast cancer and other drugs that can target the role of estrogen, progesterone and HER2 receptors, and CDK4 / 6 inhibitors belong to this category. These drugs have been approved for the treatment of ER and HER2-positive breast cancer.

Now, co-author of the study Dr. Matthew Goetz and colleagues from the Rochester Mayo Clinic Women's Cancer Program believe that the use of CDK4 / 6 inhibitors in the treatment of triple negative breast cancer may be effective. Triple-negative breast cancer cells lack estrogen, progesterone and HER2 receptors. Thus, the cancer does not respond to the treatment of the target targeting these receptors, which makes treatment more difficult. However, the team found that CDK4 / 6 inhibitors can effectively prevent triple-negative breast cancer cells spread to other parts - that is, cancer metastasis.

The study found that CDK4 / 6 inhibitors do not triple negative breast cancer cell growth. These drugs can be targeted by acting on a protein known as SNAIL to significantly reduce the spread of cancer cells to distant organs, and SNAIL can promote cancer Cell transfer. According to the researchers, their findings suggest that CDK4 / 6 inhibitors may be beneficial in triple-negative breast cancer patients.

"These findings may provide a new treatment for preventing cancer metastasis. Meo Clinic is carrying out a new study focusing on the role of CDK4 / 6 inhibitors and may inhibit the presence of women with triple negative breast cancer," Dr. Matthew Goetz says. By the way, Flarebio provides recombinant proteins of high quality including recombinant ITGB2.

A new method to treat patients with hereditary immunodeficiency

Scientists have developed a new approach using recombinant mouse proteins to repair the defective gene in hematopoietic stem cells in patients with hereditary immunodeficiency - X-linked chronic granulomatous disease (X-CGD), according to foreign media reports. Scientists transplanted stem cells into mice that had been repaired and developed into white blood cells with normal function, demonstrating that they could be used to treat patients with X-CGD disease.

X-CGD is a hereditary disease with limited therapeutic options. It is caused by mutations in the CYBB gene, which can cause NOX2 protein deficiency and damage the ability of leukocytes to resist infection. X-CGD patients in vivo white blood cells can‘t kill bacteria, so they are susceptible to infection, threatening the safety of life. In the latest study, scientists from the National Institute of Allergy and Infectious Diseases (NIAID) under the National Institutes of Health focused on mutations in the CYBB gene in which a single change in the genetic code resulted in loss of activity of the NOX2 protein.

The researchers isolated hematopoietic stem cells from two patients and used a gene-editing technique, CRISPR-Cas9, to target and repair this mutant gene. This targeted gene repair method can be defective CYBB gene sequence back to normal human sequences. It is difficult to distinguish between correct genes and normal genes. In the process, the researchers didn't detect CRISPR-Cas9 gene editing technology to produce any unexpected effect. In contrast, other methods of restoring the function of mutated genes often lead to additional changes, including genetic material additions or losses.

The researchers also transplanted stem cells from X-CGD patients into immunodeficient mice and found that these stem cells did not produce adverse effects and that they could differentiate into leukocytes and produce functional NOX2 for up to five months. The study published in the journal Science Translational Medicine suggests that although they need further research, they are now able to provide a theoretical demonstration that this gene-editing method can repair hematopoietic stem cell gene mutations caused by some minor ailments.

Scientists are planning to carry out the next step. The ultimate goal is to use this method for X-CGD patients in clinical treatment. At the same time, they also said that this gene editing method is also applicable to other blood diseases caused by single gene mutation, such as sickle cell anemia. By the way, Flarebio provides you with good-quality recombinant proteins like recombinant CDH2 at good prices.

Motor proteins pause at the ends of microtubules and stimulate their growth

Researchers at Penn State suggest that motor proteins which pause at the ends of microtubules and produce pushing forces can also stimulate their growth. According research using recombinant mouse proteins, the function of the proteins is a critical component in understanding cell division and nerve branching and growth.

Kinesins are found in multicellular organisms. They are a family of motor proteins. They act as little engines within the cells and transport molecular cargo along microtubules. The microtubules are hollow cylinders of the protein tubulin. They are dynamic and can grow and shrink when the cell change shape.

The researchers are trying to understand more about the motor and what makes the sequences unique since they carry out so many vital functions in the cells.

There are forty-five different kinesin motor proteins in human body in all. The researchers tracked the movements of each one and found that motor pauses at the end of the microtubules. Later it produces pushing forces to slide the microtubules apart and allow the motor to grow the microtubules. Their findings are reported in Nature Communications recently. They bound microtubules to a microscope slide and added free tubulin subunits together with modified kinesin-5 motor proteins. The results showed that the motor proteins added improve the rate and persistence of microtubule growth.

In conclusion, if we can terminate cancer cell division, new approaches in treatment will come into being. Therefore, understanding more about how kinesin-5 influences microtubule dynamics and its importance in properly segregating genetic material in cell division is of great concern. By the way, Flarebio offers high-quality recombinant proteins like recombinant App at competitive prices.

New class of DNA repair enzyme has been discovered

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

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

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

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

Virus cells can change into animal cells or plant cells

When a virus hijacks a bacterial cell, it quickly destroys the cell's normal structure including its DNA and then constructs a new structure which is very similar to the nuclei in animal, human and plant cells, according research using recombinant rat proteins.

According to the British Daily Mail, when a virus infects living cells, it will hijack and adapt cells to make it a virus manufacturing plant. At present, the United States University of California scientists have first discovered that the virus cells can change into animal cells or plant cells, promoting their evolution into a complex form of life.

This may be the first time scientists have discovered how complex organisms are evolving, and research shows that when a virus hijacks a bacterial cell, it quickly destroys the cell's normal structure, including its DNA. It then forms a new structure very similar to the nuclei of animal, human and plant cells.

The nucleus is the genetic control center for "higher" biological cells, which had never been found in bacterial cells, suggesting that higher-grade cells evolved for the first time in ancient interactions between bacteria and viruses. We know that virus work enters the host cells by inserting their genetic materials, allowing the virus to replicate DNA.

The final cells to form a new complete virus can infect other cells. The latest research report has been published in the journal Science. Research Group from California in the United States said they carried out fluorescent markers on virus proteins.

Researchers then used a video microscope to observe real-time changes in bacterial host cells during viral infection. They found that different viral proteins bind together inside bacterial cells, forming a functional mechanism much like the nucleus of human cells. Flarebio provides you with good-quality recombinant proteins such as recombinant Ntrk1 for your research.

To better understand the expression and regulation of SRSF2 in human hepatocellular carcinoma

The international academic journal Cancer Research has just published the latest research progress in an article titled "SRSF2 regulates alternative splicing to drive hepatocellular carcinoma development", and the study was completed by Feng Ying Study Groups from the Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. This study through recombinant horse proteins showed that splicein SRSF2 can promote the development of hepatocellular carcinoma by regulating the selective splicing of tumor-associated genes.

SRSF2 is a member of the classical SR family of proteins that not only regulates alternative splicing of genes, but also activates transcriptional processes. Previous studies in the Feng Ying group showed that the SRSF2 gene was knocked out in the liver, leading to delayed growth, severe liver damage, hepatocellular degeneration and severe hepatocellular fibrosis and indicating that SRSF2 protein plays an important regulatory role in the process of maintaining the liver. However, the expression and regulation of SRSF2 in human hepatocellular carcinoma is still not clear.

Under the guidance of Feng Ying, Dr. Luo Chunling and other samples of 90 pairs of liver cancer by tissue microarray study found that SRSF2 protein in patients with hepatocellular carcinoma samples showed high expression of the trend, and the protein expression and pathological grade of liver cancer and the patient's prognosis showed a significant correlation. The results showed that SRSF2 could promote the growth of hepatocellular carcinoma cells, and the function of SRSF2 was mainly dependent on splicing regulation of many genes downstream. SRSF2 regulates the alternative splicing of target genes GCH1 and STK39, leading to increased expression of splice isoforms that promote hepatocarcinoma cell growth, which is associated with the malignancy of HCC. In splicing mechanism, SRSF2 can enhance the exon access and inhibit the exon access dual function.

This study shows that splicein SRSF2 plays an important role in the development and progression of hepatocellular carcinoma by regulating alternative splicing of genes such as GCH1 and STK39. This work not only contributes to the understanding of the pathogenesis of HCC, but also provides a new target and ideas for diagnosis and treatment. Flarebio provides you with superior recombinant proteins including recombinant Aoc3 at good prices.

New therapy of multiple myeloma: to inhibit EZH2

In a study using recombinant dog proteins which is published in the scientific journal Oncotarget, researchers from Uppsala University showed how protein EZH2 affects the development of multiple myeloma and that EZH2 can be used as a novel strategy for treating the disease. Multiple myeloma in the form of tumors is still incurable today, and it is a challenge to improve treatment.

Researchers at Uppsala University have previously shown that abnormal chemical modification of DNA-associated proteins (histones) that regulate gene expression patterns can be a potential underlying mechanism for the development of multiple myeloma. The researchers studied the protein EZH2, which involves chemical histone modifications and reduces the survival of tumor cells by treating tumor cells with a substance that specifically inhibits EZH2.

In a recent study, Professor Helena Jernberg discovered a new mechanism at the Department of Genetics and Pathology Immunology that could explain the tumor-promoting effects of EZH2 in multiple myeloma. The researchers analyzed the activity of a large number of genes in tumor cells that had been treated with EZH2 inhibitors, and they found four important oncogenes with lower activity.

"The role of oncogenes in cancer development is to enhance the survival of cancer cells, but not death. In the case when cells can't work, they continue to divide and proliferate. In our study, we have identified four oncogenes. Compared with the control cells, cells treated with the EZH2 inhibitor showed lower activity. And the four genes have previously been shown to be associated with the development of multiple myeloma, confirming our previous finding that EZH2 inhibitors can be used as the treatment of multiple myeloma," Helena Jernberg Wiklund said.

But the researchers were perplexed by the fact that inhibition of EZH2 could reduce the activity of oncogenes. Chemical histone modifications carried out by EZH2 result in lower activity of the affected genes. Thus, inhibition of EZH2 should result in a decrease in the level of chemical modification, which in turn should lead to increased gene activity.

"The answer is that genetic factors called microRNAs have increased activity in the two microRNAs in cells treated with EZH2 inhibitors, and we believe that oncogenes are regulated by these microRNAs. And then when EZH2 is inhibited, histone modifications at the microRNA gene decreases, which leads to increased synthesis of microRNAs and in turn reduces the activity of oncogenes. It is a completely new mechanism for the effect of EZH2," Helena Jernberg Wiklund said. Flarebio provides you with recombinant proteins of good quality such as recombinant ITGB5 at good prices.

Get to know how enhancer regulates gene transcription

As a non-coding region of a DNA sequence with a specific transcription factor binding enhanced gene transcription, enhancer enhances the expression of the target protein gene in a long distance. Scientists at the University of Pennsylvania have shown through recombinant rat proteins that the mysterious non-coding RNA-enhancer RNA binds to CBP (transcription coactivator) to regulate histone acetylation, controlling gene expression and protein biosynthesis.

In cells, DNA is transcribed into RNA and used for protein biosynthesis. Most genomes are transcribed into RNA, but only a fraction of the RNA actually comes from the protein coding region of the genome. Non-coding region can't transcribe messenger RNA, but it can regulate the expression of genetic information. Although non-coding region can't encode proteins, it is indispensable for expression of genetic information.

Why are non-coding regions not being transcribed? How can their function be achieved? With these questions, Shelley Berger at the University of Pennsylvania's Institute of Epitemology and Daniel Bose, a postdoctoral fellow in her lab, are working on the regulation of gene expression in enhancers. Enhancers increase the rate of protein gene expression over a long distance, so cells can synthesize more of the desired protein molecules. The mysterious non-coding RNA, known as enhancer RNA (eRNA), is transcribed from the enhancer sequence. Although these are important for promoting gene expression, how they achieve this function is completely unknown.

Their work revealed these elusive eRNAs: CBP, an enzyme that activates enhancer transcription and binds directly to eRNAs. CBP modulates acetylation to control gene expression patterns in vivo, reducing the affinity of histones to DNA and releasing chromatin to promote transcription. This result was published in the journal Cell on January 12.

"Fundamentally, this is an important science because we show that enhancer RNA plays a key role in guiding the protein synthesis in the whole genome," Berger said. "We identified in the whole genome that enhancer RNA is the most common type of RNA that binds to CBP and that by performing this interaction, eRNAs play a key role in regulating CBP activity and gene expression." Flarebio provides you with superior recombinant proteins including recombinant ITGB5 at good prices.

iPS cells help to treat retinitis pigmentosa

Researchers in Japan have found through recombinant human proteins that after retinitis pigmentosa degeneration in mice transplanted by the induction of pluripotent stem cells (iPS cells) cultured cells, some mice restored the ability to perceive light. The results bring new hope of light for the retinal pigmented patients.

Retinitis pigmentosa is a hereditary disease. The retina which can respond to light in the visual cells gradually disappear, resulting in vision degradation and severely blindness. There is no effective cure.

Japan's Institute of Physical and Chemical Research said a research team at the Institute of Multi-Cell System Research Center using experimental mouse iPS cell cultured and obtained visual cells and transplanted to the eyes of mice suffering from retinitis pigmentosa blindness.

Researchers conducted electric shock to test visual recovery in mice through light. In the experiment, the mice were exposed to light for 5 seconds without electric shock. The results showed that about 40% of the mice receiving single-eye transplantation responded to light and avoided electrical shock, while those not receiving transplantation did not avoid electric shock.

According to the researchers, the visual cells they transplanted to mice were less than 5% of all cells. If transplanted a larger range of visual cells to retinal, the ratio of mice restoring vision may be higher.

The relevant papers have been published in the online edition of the journal Stem Cell Report in United States. The researchers plan to apply for human clinical trials within two years further on the basis of confirmation of safety. Flarebio provides you with superior recombinant proteins like recombinant COLEC12 at good prices.

The dual life of cancer protein Dab2

According to research using recombinant mouse proteins, sometimes proteins play more roles than we expect. For example, Dab2 has been considered to be associated with cancer. This molecule is associated with a series of signaling proteins called the Ras-MAPK pathway. In many cancers, the components of Ras-MAPK mutate and begin to tell cells to grow out of control.

Dr. Xiang Xi Xu (Michael), a professor of cell biology at the University of Miami's Miller School of Medicine, discovered the Dab2 protein more than 20 years ago and has been studying its relationship with cancer since that time, according to researchers at the Sylvester Comprehensive Cancer Center in the United States. But now he has found that Dab2 has always been very low-key secret - it may have an important public health impact on the fight against obesity. In a study published in Scientific Reports, Xu's lab found that young mice without Dab2 did not experience weight gain when ingesting too much food. "These mice look normal and everything seems good unless we give them a high-fat diet," Xu said. "They just do not get fat."

The underlying mechanism may be around adipose-derived stem cells: immature cells, which can be split into more stem cells or differentiated into mature adipocytes. In normal mice, Dab2 inhibits Ras-MAPK, which in turn promotes a protein called PPA R. It helps in the differentiation of adipose-derived stem cells into mature adipocytes. Eliminating Dab2 can shorten this process.

Normal mice fed a high-calorie diet gained weight, knocking out Dab2 to keep mice slim - but only temporarily. As the mice mature, the metabolic effects dissipate. At six months, the Dab2 deletion had little effect. Xu believes that this is because mice (and humans) lose fat stem cells at maturity. This early impact may help to explain "why early weight problems may persist into adulthood and why many adults are so difficult to lose weight".

"Dab2 controls a group of adipose-derived stem cells that are slowly disappearing," says Xu. "It appears that children are particularly susceptible to eating, and they may increase the number of adipocytes and fat cells at a young age, and they can still make fat later in life. But the existing fat cells are growing, and childhood habits may affect adults, making them more prone to obesity.

From a public health perspective, these findings may reinforce the importance of "guiding children away from high-fat diets". This role of Dab2 has been identified and may lead to new drug strategies to combat childhood obesity as the protein may be an attractive target for drug development. By the way, Flarebio provides you with high-quality recombinant proteins including recombinant CDH2 for your research.

The key gene which promotes breast cancer development

Why does breast cancer develop? Why do some patients resist the established treatment? Researchers at the University of Basel have gained new insight into the molecular processes of breast tissue. Through recombinant human proteins, they identified the tumor suppressor gene LATS as a key participant in breast cancer development and resistance in therapy. The findings were published in the January 10 issue of Nature.

About one-third of patients do not respond to treatment or produce resistance. So far, it has not been possible to accurately predict which patients will respond to this treatment because scientists have not yet fully understood their underlying molecular mechanisms. In a comprehensive molecular study, a team of scientists led by Professor Mohamed Bentires-Alj from the Department of Biomedical Sciences at the University of Basel now has identified an important participant called LATS. They demonstrated how this enzyme works with other proteins and how it affects the development and treatment of breast cancer.

Researchers are working on genes that inhibit the normal growth of cancer cells. In particular, they studied the tumor suppressor genes LATS1 and LATS2. Once the LATS is removed, the process in the breast tissue changes. After removal of LATS, the number of luminal precursor cells in the mammary gland epithelium increased. Luminal progenitor cells are the origin of most types of human breast cancer cells. "LATS balances the fate of cells in mammary tissue. And when it does not, the balance is broken, causing tumors to develop," Bentires-Alj explains.

In healthy breast tissue, LATS brings together estrogen receptor α and protein degradation mechanisms. Without LATS, the receptor can no longer be properly degraded, which has an adverse effect on cancer therapy. "We demonstrated that LATS-free cancer cells no longer respond to Fluvestrant, an agent that promotes the degradation of these estrogen receptor antagonists," said Bentires-Alj.

The removal of LATS also stabilizes the proteins YAP and TAZ, both of which are upregulated and promote cell proliferation in many cancers. "As we gain new insight into the molecular processes of healthy breast tissue, we now have a better understanding of how cancer cells are expanded, and why certain tumors are resistant to treatment," Basel scientist Bentires-Alj concluded. Flarebio offers recombinant proteins of good quality like recombinant CDH2.

Scientists have successfully analyzed key HIV structure

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

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

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

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

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

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

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

Scientists have found the method of wound healing without scars

Researchers have figured out how to make new wounds heal by replacing them with new ones instead of the usual scar tissue method through recombinant dog proteins. Before this, mammals want wound healing without scar is considered impossible.

"In essence, we can manipulate wound healing so it can regenerate the skin instead of scars," says George Cotsarelis, a professor of dermatology at the University of Pennsylvania. "The secret to achieving this goal is to regenerate hair follicle, and then the signal released by hair follicle will promote the regeneration of fat.

Scientists have found that existing myofibroblasts can be transformed into adipocytes, suggesting that when a wound heals, the scar tissue can be transformed into regenerated skin. Scientists previously thought that only fish and amphibians could do that. "These findings suggest that we have an opportunity to influence tissue regeneration rather than waiting for scar formation," said Maksim Plikus of the University of California, Irvine.

Previous research by the team showed that fat cells and hair follicles in regenerated skin developed separately but did not develop independently, and hair follicles were always the first to develop. Researchers suspected that the growth of hair follicles can help the regeneration of fat cells, so they induce hair follicles in mice and laboratory-cultured human skin scar tissue growth. This thing will never happen naturally, because there is no scar tissue inside the hair follicle. They found that once the hair follicle had been formed, it could release the signaling protein, BMP, which in fact turned scar fibroblasts into adipocytes. If hair follicles are induced to grow at the wound healing, the result will be that the post-healing skin is nearly the same as before.

"It is generally believed that myofibroblasts can’t become other types of cells, but our work suggests that we have the ability to influence these cells and that they can effectively and stably transform into adipocytes," Cotsarelis said.

It should be noted that the experiment is only in the proof-of-concept phase, which is effective in mouse and human skin samples, but the effect on the living human remains to be checked. Flarebio provides superior recombinant proteins including recombinant CDH15 at great prices.

To revolutionize the treatment of metastatic uveal melanoma

New research at the University of Liverpool has identified the role of specific proteins in the human body and found that they can help to prevent eye cancer by initiating cancer "cell suicide". The new findings obtained through recombinant dog proteins may help to revolutionize the treatment of metastatic uveal melanoma (UM) - a disease caused by pigment cells (melanocytes) in eyes - and there is currently no effective treatment.

Metastasis is that cancer or other diseases spread from one part of an organ or the body to another, rather than the part directly connected to it. This is the case in about half of all UM patients. Although rare, UM is the most common primary eye cancer in adults. Although primary tumors can usually be treated very effectively, as many as 50% of patients have metastases in the liver, and there is no effective treatment for such metastases.

Dr. Luminita Paraoan from the Department of Ophthalmology and Visual Science at the Institute of Gerontology and Chronic Disease, University of New York, published a new study in the British Journal of Cancer that identified the role of a protein called p63 in UM. Chromosome 3 is one of 23 human chromosomes. People usually have a pair of chromosomes. A portion of chromosome 3 contains the gene of protein p63. Unfortunately, people with aggressive (anti-apoptotic) cells do not have this part, so there is no p63 protein.

Dr. Paraoan found that if the p63 gene is used in combination with another gene called p53, it can effectively target UM and induce cancer cells to undergo apoptosis. The p53 gene is a class of genes from a so-called tumor suppressor gene that is mutated in cancer cases. Tumor suppressor genes are protective genes. Typically, they limit cell growth by monitoring cell division into new cells, repairing damaged DNA and controlling the rate of cell death.

When a tumor suppressor gene is mutated, for example in a cancer case, the cell grows uncontrollably and may eventually form a mass called a tumor. Thus, p53 itself is ineffective in activating apoptosis in UM. "This study highlights for the first time the condition that p63 triggers apoptosis in UM," said Dr. Luminita. "Our results have broad implications for other escape cell-mediated conditions or cancer, and we hope to demonstrate a benefit to the treatment of cancers which have resistance to current chemotherapy and radiotherapy." Flarebio offers recombinant proteins of good quality like recombinant TLR2 at great prices.

How does inheritance hearing loss happen?

Japanese researchers have used an inducible pluripotent stem cell (ips cell) from a patient with hereditary hearing loss and recombinant human proteins to develop inner ear cells and compared them with healthy human inner ear cells, finding the pathogenesis of this disease. This study is also expected to be used to find other treatment of hearing impairment.

Goitre - deafness syndrome is a rare congenital thyroid hormone organic synthesis disorders. It is an autosomal recessive inheritance with goiter and sensorineural deafness as the main clinical symptoms. Patients tend to develop hearing impairment from an early age and may have a language delay. The abnormalities of genes which control and synthesize protein Pendrin are considered to be pathogenic, but the specific pathogenesis is unclear.

Researchers at Keio University and other institutions used patients' blood to produce ips cells, and then they were induced and differentiated into inner ear cells. The researchers compared the inner ear cells differentiated from healthy ips cells. The researchers found that the Pendrin proteins in the inner ear cells differentiated from ips cells showed abnormal agglutination. The cells are easy to die, which is similar to the pathogenesis of Alzheimer's disease.

Ips cells are stem cells transformed by somatic cells through induced factors after treatment, having the possibility of developing into a variety of tissue cells.

Researchers in the cell experiments also found that an immunosuppressive agent sirolimus can effectively inhibit the inner ear cell death. In addition, the use of ips cell culture in patients with inner ear cells are also expected to find other treatments for hearing impairment, and the researchers prepared to conduct further research on this. Flarebio provides you with superior recombinant proteins including recombinant TLR2 at competitive prices.

New way of identifying subtypes of Alzheimer's disease

Recently, scientists have published an article on early identification of the onset of progressive Alzheimer's disease in the journal Nature which also publishes some other studies on recombinant dog proteins, providing some basis for individual and precise treatment of Alzheimer's disease.

Researchers at the National Institutes of Health and the College of Neurology of the London College of Medicine have found that the type of fibrogenesis is associated with subtypes of Alzheimer's disease. A study published by them on nature described: the formation of brain tissue deposition of amyloid fibrils can reflect the physiological characteristics of Alzheimer's disease. The study found that the type of fiber with the degree of disease and pathological subtypes would show different morphological or size differences. According to this, we can classify the types of early Alzheimer's disease. This is a time-consuming and labor-intensive experimental project, so the relevant research is rare. To investigate the problem, the authors collected 37 tissue samples from the brain tissue of 18 dementia sufferers of the late Alzheimer's disease. They used magnetic resonance techniques to detect the deposition of these brain β-amyloid forms, while the clinical classification of these patients was compared. (Some patients were diagnosed with rapid progression; some patients were diagnosed as classic; and some patients had posterior cortical atrophy). The researchers found that classic patients with cerebral cortical atrophy have the same pattern with patients with cerebral β-amyloid deposition. However, the pattern of amyloid deposition in patients with rapid progression is often different from that of other types of patients.

The researchers believe that the rapid progress of Alzheimer's disease has a special β-like protein deposition pattern, resulting in the condition that the type of brain tissue in patients with fibrous lesions of the size and morphology are different from other types. This helps early identification of rapidly progressing Alzheimer's disease patients and gives them timely treatment. Researchers have also admitted that because the number of specimens is too small, the mechanism is not clear. Further studies remain to be carried out, and greater progress will be made. Flarebio provides you with superior recombinant proteins like recombinant ECEL1 at good prices.

To treat anti-NMDA receptor encephalitis with this method

Recently, German researchers have discovered through recombinant human proteins that a drug for the treatment of blood tumors can be used for the treatment of anti-NMDA receptor encephalitis, effective treatment of critically ill patients.

Anti-NMDA receptor encephalitis i.e. anti-N-methyl-D-aspartate receptor encephalitis, is an autoimmune disease. Schizophrenia, epilepsy, movement disorders and other symptoms caused by brain inflammation may lead to death. In recent years, this encephalitis mainly happens in females gained attention by the medical field.

Researchers at the Charité University Hospital in Berlin and at the German Neurodegenerative Disease Research Center in Berlin, Germany found that the standard of care available to critically ill patients with encephalitis was limited and that the addition of the drug bortezomib was based on standard therapy, resulting in the quick improvement of five critically ill patients. Bortezomib is a proteasome inhibitor originally used to treat rare blood tumor-plasmacytomas.

NMDA receptors play an important role in the process of brain signaling. But plasma cells produce antibodies that block the normal functioning of NMDA receptors in patients with NMDA receptor encephalitis. Bortezomib can effectively kill plasma cells so that antibodies can reduce the radical treatment of such encephalitis and bring new treatment options for critically ill patients.

The study was published in the new issue of international academic journal Neurology. By the way, Flarebio offers good-quality recombinant proteins including recombinant ITGB5 for your research.

Nature Communications: new target of atherosclerosis has been found

Recently, a team from Yale University found a protein that plays an important role in intravascular deposition of low-density lipoprotein (LDL) cholesterol, which provides an innovative medical approach to block LDL deposition. To prevent or slow down blood vessel obstruction leading to heart disease. The research is published in the journal Nature Communications, which also publishes other studies on recombinant human proteins.

Cardiovascular disease caused by atherosclerosis is the world's first major cause of death. Atherosclerosis occurs because lipoproteins, especially LDL, bind to fat and cholesterol in the bloodstream and transport them through the endothelial cells that make up the inner walls of the blood vessels, whereas the deposition of fats and cholesterol in the subendothelial region results in Atherosclerosis of the important reasons.

At present, the most effective therapy to prevent such diseases is to lower the level of LDL in the blood, which reduces the likelihood that LDL lipoprotein particles enter and reside in the vessel wall. However, the molecular mechanisms by which LDL is transported across the vascular endothelium have not been fully elucidated. For a long time, scientists believe that LDL receptors are responsible for intracellular transport of LDL function. However, some people who don't have LDL receptors in the body still produce high levels of LDL deposition, which mechanism is still an unsolved mystery.

To find out the mechanism of LDL transport, researchers at Yale University used RNAi libraries to screen more than 18,000 genes. They focused on genes that affect the transport of LDL into endothelial cells. The results show that a protein called ALK1 can help LDL to the intracellular transfer. ALK1 binds directly to LDL and promotes LDL through endothelial cells into subendothelial tissue through a specific endocytic pathway, rather than introducing LDL into lysosomal degradation. If the ALK1 gene is specifically knocked out in the endothelial tissue of the mouse, the LDL level of the vascular endothelium is reduced.

"We found that ALK1 protein can bind to LDL, which means it may trigger early atherosclerosis," said William C. Sessa, professor of communication at the University of Yale. "If we find small molecules or antibodies that block ALK1 protein, then it may be used in conjunction with other lipid-lowering therapies to reduce the risk of atherosclerosis." By the way, Flarebio provides you with high-quality recombinant proteins like recombinant NPP1 at good prices.

This microprotein existing in P-body is also vital to our body

In the genome of human body, there is a large number of genes small open reading frame (smORF). They encode too small proteins that most of these genes have not been annotated, not to mention the function of the protein they translate. These "microproteins" are difficult to detect. Therefore, scientists at Yale University and the Salk Institute have adopted a set of special methods through recombinant mouse proteins. They first cleared the larger volume of protein in the cell and then analyzed the amino acid sequence of the remaining protein components using liquid chromatography-mass spectroscopy proteomics and designed the biology Information algorithm. The results identified more than 400 such microproteins and their genes. The results have been published in the recent issue of the journal Nature.

Among the microproteins over 400, the scientists have performed a functional study of a protein that is involved in mRNA degradation in the cell and recycling excess mRNA, preventing mRNA from continuing to produce specific proteins that are no longer needed. Thus, the process of gene expression in the cell regulation is very important. However, for this mechanism, we didn't know that there is a "little" protein which plays a key role.

The protein, called Nobody, is indeed "obscure" as its name looks like. However, Nobody's actual full name is non-annotated P-body dissociating polypeptide, which means "un-annotated P-body dissociation polypeptide" and has high evolutionary conservatism.

The researchers found that Nobody exists in the P-body and has interaction with a variety of protein components (such as cap enzyme). P-body is consisting of mRNA and a variety of proteins, and it completes the mRNA degradation recovery process in the first step - dacapping. Experiments show that the level of Nobody in the cell is negatively correlated with the number of P-bodies, and abnormal changes in Nobody level would interfere with the normal mRNA recovery process.

"Although Nobody has not yet been associated with any specific disease, other micro-proteins have this potential," said Alan Saghatelian, professor of communication at the Salk Institute and one of authors of the paper. "For the search and analysis of these proteins, to reveal its role in physiological and pathological processes will be an exciting frontier in molecular biology." Flarebio offers high-quality recombinant proteins like recombinant NPP1 at competitive prices.

New cardiac stem cells which have great treatment potential

Researchers from North Carolina State University and the First Affiliated Hospital of Zhengzhou University in China have developed a new version of a new cardiac stem cell (CSC), according to a new study involving recombinant mouse proteins and it has been published in the International Journal of Nature Communications. These synthetic cells can provide therapeutic potential compared to natural stem cells, while reducing the risk of disease associated with stem cell therapy. In addition, the new stem cells developed by the researchers also have some stability, and this technology is expected to help to develop other types of stem cells.

Stem cell therapy can play a role in promoting endogenous repair of the body, that is, it can repair damaged tissues by secreting paracrine factors, including proteins and genetic material. When stem cells therapies can be effective in the treatment of disease, they often tend to induce tumor growth and immune rejection. What's worse, these stem cells themselves are very fragile. Before being used, they need to conduct a series of important processes.

"We developed a new version of heart stem cells, and these stem cells can be used in a variety of off-the-shelf applications," said Ke Cheng, co-author of the study. Researchers have developed a cell-derived microparticle (CMMP) that utilizes poly (lactic-co-glycolic acid) (PLGA). PLGA is a biodegradable and biocompatible polymer. Then researchers obtained growth factor protein from human heart stem cells and added this growth factor protein to PLGA, finally successfully covering these PLGA particles with the heart stem cell membrane. "We can package 'cargo' and stem cell shells into biodegradable particles," Cheng said.

In vitro, both CMMP and heart stem cells have been shown to promote cardiac muscle cell growth. CMMP has also been tested in a mouse model of myocardial infarction and found that CMMP binds to cardiac tissue and can promote growth after the onset of heart disease, and this effect is considerable with the repair role of heart stem cells. Due to a special structure, CMMP can't replicate, which reduces the risk of tumor formation.

The researchers pointed out that these new synthetic cells have the same principle with inactivated vaccines. While outer membrane structure can also help to bypass the body's immune response, which combine with the heart tissue, releasing special growth factors for repair. But these new stem cells can't self-replicate, so it will be able to repair the body tissue to produce a stable effect while at the same time with lower risk. These new stem cells are more durable than human stem cells and are well tolerated by repeated freezing and thawing. Scientists don't necessarily have to acquire these cells from human cells. The development of these cells is also applicable in other stem cells.

Finally, the authors hope that this study will provide a new basis for the development of more novel stem cell products in the future, and the development of new stem cell products will of course provide beneficial stem cell therapy for patients while reducing the risk of other complications. Flarebio provides you with recombinant proteins of good quality such as recombinant CDH2.

Some apolipoproteins are associated with type 2 diabetes

The proportion of apolipoprotein (apo) CIII and apoCIII to apoA1 is associated with type 2 diabetes (T2D), according to a study published in the December 28 issue of Diabetes Care, which also has some other studies on recombinant human proteins.

Dr. Adela Brahimaj and colleagues from the Erasmus University Medical Center in Rotterdam, the Netherlands, and used data from 971 individuals from the population-based Rotterdam study to examine the role of apolipoprotein in the risk of type 2 diabetes. They examined the association of high-density lipoprotein cholesterol (HDL-C), apoA1, apoCIII, apoD and apoE, and the ratio of apolipoprotein to apoA1 and T2D risk.

The researchers found that at a median follow-up of 13.5 years, 110 people developed diabetes. Apolipoprotein E, apoA / apoA1 ratio, apoE to apoA1 ratio and apolipoprotein score remained significant after adjusting for age, sex, body mass index, diabetes maternal history, hypertension, alcohol use, smoking, diabetes mellitus. The prevalence of cardiovascular disease was associated with a serum lipid-lowering agent (odds ratios of 0.74, 1.65, 1.36, 1.72, 1.88 and 1.6 for each standard deviation of natural logarithmic conversion). After adjustment for triglycerides in the final model, only apoCIII and apoCIII-to-apoA1 ratios remained significant (hazard ratios, 1.42 and 1.56, respectively).

"Serum apoCIII levels and apoCIII-to-apoA1 ratios are associated with incident type 2 diabetes," the authors write. They are independent of known risk factors and are stronger than HDL-C levels. Flarbio provides high-quality recombinant proteins like recombinant Itgb2 at competitive prices.

Fstl1 protein is capable of inducing cardiac muscle cell regeneration

American scientists have conducted biological research on mice and pigs through recombinant rat proteins, and the research showed that a protein called follistatin-like protein 1 (Fstl1) is capable of inducing cardiac muscle cell regeneration after an adult mammalian heart attack. The results suggest that repair of epicardial Fstl1 expression may be the effective way to stimulate the heart "rebirth", opening up a new treatment.

The mammalian heart lacks the ability to fully self-repair a significant number of damaged cardiomyocytes after a heart attack, and the medical community has not been very clear about the factors limiting myocardial regeneration. Fstl1, a member of the extracellular matrix protein family, is found in almost all mammals and is secreted by many cells. It has been shown that Fstl1 possesses the ability to regulate cell proliferation, differentiation, apoptosis and metabolism. But the biological function has not been fully revealed.

This time, Praz Ritz-Rozno of Stanford University and her team showed that Fstl1 is expressed mainly in the epicardium in healthy hearts. Epicardium is a layer of the membrane wrapped around the heart. But after a heart attack, epicardial Fstl1 expression will be missing. The team found that when placing a patch of biochemically mimicked epicardial tissue on the heart of damaged mice and pigs, as a source of Fstl1, it can induce proliferation of cardiomyocytes and improve the function of the heart and their survival in these animal models.

The results of this study suggest that restoration of Fstl1 expression in the epicardium may be an effective way to regenerate cardiomyocytes after a heart attack, thus developing new therapies. Research related papers were published in the 17th issue of the British journal Nature. By the way, Flarebio provides you with superior recombinant proteins including recombinant CDH15 at good prices.

New method of improving obesity is coming!

Recently, the international academic journal Diabetes published a study titled "Deletion of ATF4 in AgRP neurons promotes fat loss mainly via increasing energy expenditure" online by Guo Feifan research group from Institute of Nutrition, Shanghai Institute of Life Sciences, Chinese Academy of Sciences. This study found through research using recombinant dog proteins that activation of transcription factor 4 (ATF4) regulates energy balance and lipid metabolism in hypothalamic-specific neurons of AgRP neurons, providing a potential drug target for the treatment of obesity and related metabolic diseases.

In recent years, both in developing and developed countries or in adults and children, obesity are widely prevalent, and it is closely related to a series of metabolic syndrome such as diabetes, fatty liver, dyslipidemia and cardiovascular diseases, becoming a great threat to human health. Therefore, the study of obesity development mechanism is particularly important. Changes in body weight are caused by imbalances in energy intake and energy expenditure and the central nervous system, especially the hypothalamus, play a key role in regulating energy balance.

Our brain contains a variety of specific types of neurons which have different functions, regulating the body's behavior and metabolic balance. The arcuate nucleus (ARC) of the hypothalamus contains two types of neurons that regulate metabolism: one is appetite-suppressing neurons, such as pro-opioid (POMC) neurons; the other is appetite-promoting neurons, including Neuropeptide Y (NPY) and gerbil peptide gene-related protein (AgRP) neurons. AgRP neurons can release the AgRP protein and inhibit the activity of POMC neurons, thus promoting increased food intake; it also affects energy consumption by adjusting the sympathetic nervous system or leptin sensitivity. The study of how specific neurons such as AgRP regulate energy metabolism will provide an important theoretical basis for the discovery of the etiology and treatment of obesity.

Postdoc DENG Jia-li and Ph.D. student FEI Fei used inducible gene knockout techniques to specifically knock out ATF4 in AgRP neurons of adult mice under the guidance of Guo, finding that these mice were thinner with insulin sensibility and leptin sensibility improved. At the same time, the experimental mice reduced food intake and increased energy consumption, improving the body heat. After high-fat diet, ATF4 mice with AgRP-specific knockout were resistant to high-fat-induced obesity, insulin resistance and fatty liver. Further study of its mechanism of action found that ATF4 can be combined with the promoter of FOXO1 to directly regulate its expression. After injection of FOXO1 adenovirus in the arcuate nucleus of the hypothalamus of the knockout mice, the fat content of mice significantly increased.

In summary, the study found the important function of ATF4 in the hypothalamic AgRP neurons to regulate energy balance and lipid metabolism, suggesting that the treatment of obesity and metabolic diseases, ATF4 may become a new drug target. Flarebio provides you with high-quality recombinant proteins like recombinant PIGR at competitive prices.

FANCM mutations should be included in risk assessment of breast cancer

Eric Hahnen of the University Hospital of Cologne, Germany, conducted a case-control study screening in FANCM function-deleteda mutations in familial breast cancer patients and ovarian cancer patients and control group using recombinant human proteins. Because the FANCM gene is associated with an increased risk of breast or ovarian cancer and the FANCM protein and its binding protein FAAP24 are involved in the DNA damage response, the gene plays an important role in cancer. The findings, published in the December 29 issue of JAMA Oncology, found that FANCM mutations are more common in patients with familial breast cancer risk, especially in triple-negative breast cancer or younger patients. This suggests that FANCM mutation detection should be incorporated into the risk assessment of breast cancer.

Hahnen et al. have estimated that the frequency of cumulative carriers in familial breast cancer is 1.03%. Based on this, they showed a weak but significant association between FANCM mutation and familial breast cancer. The researchers then found that the incidence of familial breast cancer before the age of 51 and FANCM mutations have a stronger association between the cumulative frequency of the subgroup carriers 1.22%. In contrast, the cumulative carrier frequency for the subgroup of patients who developed disease after the age of 51 was 0.613%.

The researchers also found that FANCM mutations were more common in patients with triple-negative breast cancer. Among all the 215 triple-negative breast cancer cases, 4 had FANCM mutations and the cumulative carrier frequency was 1.86%. The researchers didn't find a link between FANCM and ovarian cancer, and they suggested that they should be analyzed further on a larger scale.

The shortcoming of this study is that researchers are only concerned with familial breast cancer and may therefore be biased for selection. In the following study, they may analyze all cases of breast cancer and may be stratified according to whether the case is premature or triple negative. "Based on this and previously published research, we recommend that the FANCM mutation be placed in the diagnostic panel," the authors write. By the way, Flarebio offers high-quality recombinant proteins like recombinant Aoc3 at competitive prices.

optoDroplet provides new hopes for the treatment of protein-related diseases

In a study published in the December 29 issue of Cell, Professor Brangwynne of Princeton University developed a new tool called optoDroplet through recombinant proteins including recombinant horse proteins. This tool can analyze the physical and chemical changes in the self-assembly of membranous organelles and provide new hopes for the development and treatment of protein-related diseases by controlling the aggregation and dissolution of proteins.

The OptoDroplet is a technique that relies on photogenetics to change the behavior of proteins by exposure to light. The major component of the cell is water, and therefore it is substantially transparent. Researchers have shown that they can induce phase transitions by activating photoactivators and produce membraneless organelles. At the same time, they can simply turn off the lights to cancel the process. Increasing light intensity and protein concentration allowed the researchers to further control transformation. By altering these factors, they can determine when to form condensed liquid proteins, as well as solid-like protein aggregates that may be associated with the disease.

Using mouse and human cells, the research team spliced genes from the Arabidopsis light-sensitive protein, and blue exposure will lead to self-assembly of the protein. Proteins fused with a light-sensitive label are thought to drive phase transitions in living cells. The researchers found that they can light the protein to induce aggregation, mimicking naturally occurring in the cell condensation process. The team repeatedly made the protein to condense and then dissolve by turning on and off light. Even after many cycles, this process proved completely reversible. However, with high-intensity light or high concentrations of protein, the researchers created a semi-solid gel. These gels were initially reversible, but over time they solidified to form irreversible bulk agglomerates, similar to those found in some diseases.

An example is a protein called FUS. FUS protein is essential for cells: it helps to produce other proteins and repair damaged DNA. But a large number of mutations may make FUS protein become too sticky, leading to amyotrophic lateral sclerosis (ALS). This is a progressive and fatal neurodegenerative disorder in which the patient loses the ability to autonomously control his or her muscles and protein aggregates accumulate in nerve cells of ALS patients. These clumps may originate from the pathological aggregation of FUS or other proteins, rather than being maintained as a dynamic fluid. Huntington‘s disease and Alzheimer’s disease are also associated with protein clumps blocking cells, again demonstrating that abnormal phase transitions in cells are closely related to these protein concentrations and light intensities.

Professor Brangwynne looks forward to continuing to experiment with optoDroplet to better understand the complex behavior of cells. He also hopes that these insights will not only reveal how healthy cells work but also reveal how they are pathogenic and may ultimately cure the disease. Flarebio offers superior recombinant proteins like recombinant TLR2 at competitive prices for your research.

A research team has found a new approach to shut down CRISPR-Cas9

A recent research team has found a new approach to shut down CRISPR-Cas9 that addresses potential problems with CRISPR-Cas9 gene editing methods. The team used phage proteins, allowing more precise gene editing and giving the researchers the ability to disable the entire system. Details have been published in the December 29 issue of the Journal of Cell, which also publishes some other studies on recombinant dog proteins. Prior to this, in another study published by Cell, scientists discovered the first known "off switch" for CRISPR - Cas9 activity.

CRISPR-Cas9 is a method used by scientists to edit the genome. Cas9 is an enzyme that cleaves DNA fragments so that they can be replaced. The CRISPR-Cas9 system is naturally occurring in bacteria and is a method for combating phage and targeting bacteria only. It is able to cut and store viral DNA slices to allow bacteria to recognize phages in the future. Researchers use this system to modify the genome and repair genetic diseases. However, CRISPR-Cas9 occasionally goes wrong. In the past, scientists had no way to disable the system, leading to security issues of future human trials.

Researchers from the University of California, San Francisco have explored possible ways to inactivate the CRISPR-Cas9 system. CRISPR-Cas9 is mainly a method of fighting bacteria and viruses, but the team observed the infected bacteria. If the bacterium infects the bacterium and inserts its DNA, Cas9 tries to cut it off even if it will target the bacteria's own genome. Because the virus needs to have a live host, this will not help the virus. The team hypothesized that some phages had an anti-CRISPR protein for inactivation of Cas9. In screening the bacteria infected in this way, the team found two anti-CRISPR proteins, known as AcrIIA2 and AcrIIA4. Both proteins were able to inhibit the Cas9 enzyme. AcrIIA2 and AcrIIA4 can be used to inactivate Cas9, shutting down the entire CRISPR-Cas9 system.

The team's findings will allow scientists to better control gene editing. If the CRISPR-Cas9 system starts making mistakes, the researcher can disable it. The system can be temporarily or permanently shut down, which make the technology will more secure for final human trials. Flarebio provides good-quality recombinant proteins such as recombinant ECEL1 at competitive prices.

A new study published in the Proceedings of the National Academy of Sciences shows that a protein can promote the treatment of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, Huntington's disease and amyotrophic side, according to a new study published in the December 29 issue of the Proceedings of the National Academy of Sciences (PALS, which also publishes some studies on recombinant human proteins).

The researchers tested Nrf2 in two Parkinson's disease models, which are cells with protein LRRK2 and α-synuclein mutations respectively. By activating Nrf2, the researchers turned on several "housekeeping" mechanisms in the cell to remove excess LRRK2 and α-synuclein.

"Nrf2 coordinates the entire process of gene expression, but we don't know how important it is to regulate protein levels," says lead author Dr. Gaia Skibinski. "Over-expression of Nrf2 in Parkinson's disease cell models has a huge effect. And in fact, it's better than anything we've found to protect cells from disease."

In this study, scientists used pluripotent stem cells to produce mouse neurons and human neurons and then programmed neurons to express Nrf2 and the mutant LRRK2 or α-synuclein. Using a robotic microscope developed by Finkbena Labs, researchers tagged and tracked individual neurons, monitoring their protein levels and overall health over a period of time. They spent thousands of cells in the process of imaging a week to monitor the development and death of each cell.

Scientists have found that Nrf2 works in a different way, helping to remove intracellular mutant LRRK2 or α- synuclein. For the mutant LRRK2, the Nrf2 drives protein to aggregate into irregular clumps that can be retained in the cell without damaging it. For α-synuclein, Nrf2 accelerates protein breakdown and clearance, reducing its level in the cell.

"I have confidence in this strategy for the treatment of neurodegenerative diseases," senior author Finkbeiner said in the text. "We have tested Nrf2 in Huntington's disease, Parkinson's disease and the ALS model, which is the most effective thing we've found, and we wanted to better understand the role of Nrf2 and its role in protein regulation, based on the magnitude and extent of its effect.

Scientists say that Nrf2 itself may be difficult to target with drugs because it participates in many cellular processes, so they are now focusing on some of its downstream effects. They hope to find other roles in the protein-Nrf2 interaction to improve cell health and to find pathways that can be more easily manipulated with drugs. By the way, Flarebio provides superior recombinant proteins like recombinant ITGB5 for your research.