CUSABIO Rabbit anti-human Ephrin-B1 polyclonal Antibody(EFNB1)

Product Name: Rabbit anti-human Ephrin-B1 polyclonal Antibody(EFNB1)
Product Type: Polyclonal Antibody
Size:        100ul(144ug)
Uniprot Num: P98172
Storage: Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze.
Image: Immunohistochemistry   Immunohistochemistry of paraffin-embedded human liver using CSB-PA007465ESR1HU at dilution 1: 100Immunohistochemistry of paraffin-embedded human placenta using CSB-PA007465ESR1HU  at dilution 1:100  Immunohistochemistry   Immunohistochemistry of paraffin-embedded human liver using CSB-PA007465ESR1HU at dilution 1: 100Immunohistochemistry of paraffin-embedded human placenta using CSB-PA007465ESR1HU  at dilution 1:100

Immunoge: Recombinant human Ephrin-B1 protein (28-237aa)
Raised in: Rabbit
Species Reactivity: Human
Tested Applications: ELISA,IHC;Recommended dilution:IHC:1:20-1:200
Relevance: Binds to the receptor tyrosine kinases EPHB1 and EPHA1. Binds to, and induce the collapse of, commissural axons/growth cones in vitro. May play a role in constraining the orientation of longitudinally projecting axons. Cell surface transmembrane ligand for Eph receptors, a family of receptor tyrosine kinases which are crucial for migration, repulsion and adhesion during neuronal, vascular and epithelial development. Binds promiscuously Eph receptors residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. The signaling pathway downstream of the receptor is referred to as forward signaling while the signaling pathway downstream of the ephrin ligand is referred to as reverse signaling. Binds to the receptor tyrosine kinases EPHB3 (preferred), EPHB1 and EPHA1. Binds to, and induce the collapse of, commissural axons/growth cones in vitro. May play a role in constraining the orientation of longitudinally projecting axons.
Form: Liquid
Conjugate: Non-conjugated
Storage Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Purification method: Antigen Affinity Purified
Isotype : IgG
Clonality: Polyclonal
Code: CSB-PA007465ESR1HU
Alias: EFL-3,ELK ligand,ELK-L,EPH-related receptor tyrosine kinase ligand 2,LERK-2,EFNB1,EFL3, EPLG2,LERK2
Species : Human
HGNC: 3226
RGD: 2540
MGI: 102708

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Link:    http://www.cusabio.com/Polyclonal-Antibody/Rabbit-anti-human-Ephrin-B1-polyclonal-AntibodyEFNB1-1092125.html

E47 protein can reduce the tumor-promoting potential of pancreatic cancer cells

New research confirms that by introducing a protein called E47 can induce pancreatic cancer cells revert to normal cells. DNA sequence-specific binding E47 and control some genes associated with the growth and differentiation.

Sanford - Burnham Medical Research Institute, Dr. development, aging and regeneration projects Visiting Professor Pamela Itkin-Ansari said: "The first time we demonstrate overexpression of a gene can reduce the tumor-promoting potential of pancreatic cancer cells, they will be re-programmed original cell type.

Construction of a kind of human pancreatic ductal adenocarcinoma cell line, E47 than normal levels it produces higher. Increase in cell E47 makes arrest in G0 / G1 growth, differentiation as a return to acinar cell phenotype. In vivo studies show that, when the Recombinant mouse Baculoviral IAP repeat-containing protein 5 http://www.cusabio.com/Recombinant-Protein/Recombinant-mouse-Baculoviral-IAP-repeat-containing-protein-5-11031431.html into the mice, in comparison with untreated cancer cells was significantly decreased ability to form tumors.

Outside the University of California, San Diego Moores Cancer Center, professor, National Cancer Institute, Dr. pancreatic Special Group Co-chair Andrew M. Lowy said: "The current use of cytotoxic drugs are used to treat pancreatic cancer, the average survival time of patients after diagnosis is only is a day for six months, to improve the treatment of calculations. found that we can make these cancer cells to differentiate into a recession is not threatening phenotype encouraging.

Exercise is not the role of hormones in the body metabolism

One can control how body fat storage and use of molecules was found. This is called the iris pigment hormone, seems to amplify the energy consumption in mice after exercise, for the treatment of diabetes and obesity research and development potential to open the way. But follow-up studies have yielded inconsistent conclusions, which led many scientists to suspect that the hormone did not play a role in human metabolism. Currently, the research antibody kit questioned the reliability of a review for the iris pigment further. Such a kit is typically used to detect iris pigment.

Harvard Medical School, a cell biologist Bruce Spiegelman and colleagues describe how FNDC5 called protein is to enhance metabolism in mice. In general, muscle after exercise will produce this protein. They found that a FNDC5 fragment - brown adipocytes Iris Pigment, run more like energy is secreted into the blood stream, and enables the white fat cells store energy consumption. The researchers also found that serum iris pigment, but after a few weeks of endurance training, Iris hormone levels seem to increase.

University of London, King's College systems biologist James Timmons said the new paper changed the debate about the fundamental elements of Iris. He is also opposed to such contact FNDC5 and human movement. He said, iris pigment in the human body and there is no reliable data for the positive support, before the paper-based ELISA tests should be withdrawn. A prime ELISA Owner Iris, pointed out that in fact the size of the loop iris pigment molecules are still subject to controversy, which Rat Testosterone ELISA Kit  http://www.cusabio.com/ELISA-Kit/Rat-TestosteroneT-ELISA-Kit-107011.html  led to the laboratory in the presence of inconsistency on how to measure the hormone.

On the other hand, Spiegelman stressed that not all previous studies rely on human iris pigment ELISA kit. For example, last year, Celi reported human blood levels of the hormone mild, and have increased after exercise. The research team used a more sophisticated technique called mass spectrometry, the technology can ionize and weigh their ingredients, to identify the sample molecules.

Exon sequencing identified two familial pulmonary fibrosis-related genes

Southwest Center for Christine Kim Garcia and her colleagues added, carrying these mutations lead to telomere shortening, which can lead to diseases such occasional, extremely poor survival. Garcia and his colleagues on 99 patients with idiopathic pulmonary fibrosis have conducted exon sequencing. Then they focused on the 78 patients, they use a subset of Mouse ANGPTL3 ELISA Kit http://www.cusabio.com/ELISA-Kit/Mouse-Angiopoietin-related-protein-3ANGPTL3-ELISA-kit-64357.html its analysis and sequencing results with 2816 controls of European descent who were compared.

By focusing their study of mutations that may affect the coding sequence of a protein with a function, such as prematurely aborted transfer and splice site mutations, the researchers found, PARN and RTEL1 to achieve influence on the whole genome level role of the protein. The researchers noted that they proved by Sanger sequencing, in PARN, there are six heterozygous mutation destructive, while in the control group, do not have these mutations. The researchers added, PARN coding 3 'end of exon cutting.

However, the researchers found, PARN mutated two participants were found to contain the same origin - two of them have a common grandmother - which means, in fact, the researchers found that the five independent PARN new mutations, five mutations, still has a very important significance. All five loss of function mutants, are capable of producing CAF1 ribonuclease domain influence, this domain is conserved from yeast start to become domain, and which is also part of the cytoplasm deacetylation of crucial.

Meanwhile, Garcia and her colleagues found that five new heterozygous mutation - with two destructive and three missense mutations in the highly conserved RTEL1 - which are in pulmonary fibrosis patients have found. However, they are in the control group also found some RTEL1 mutations, but they still found a more destructive and missense mutations in conserved residues in the sequence. However, this was not sick five mutation carriers, the researchers explained that this may be due to penetrance of the disease caused by incomplete.

Analysis, the researchers also measured the separation of leukocytes from the circulation out of whole genomic DNA telomere length using a terminal fragment length and qPCR. They found that a mutation PARN and RTEL1 crowd than they did a spouse-related impacts, the average length of their telomeres shorter. Those who do not inherit the mutation RTEL1 PARN and family members, compared to their spouses, they also have shorter telomeres, but its length than those associated mutations relatives carry longer. The researchers noted that, in line with the inheritance of telomere length and epigenetic rule.

How does bacteria to stealth?

Institutions such as Stanford University researchers found that the reason why some bacteria "stealth", from a specific protein dominant bacterial cell wall, "Metamorphosis", in order to evade the body's immune system, "detection" or antibiotics "attack."
1950s, Nobel laureate Joshua Lederberg discovered that some bacteria cell wall will fall off, no longer presents a unique shape, so that the immune system, "oversight"; after a period of time, these bacteria will regain the cell wall restore the original shape again have the ability to infect humans round.
The presence of the cell wall, bacterial protective effect, but also the release signal, to trigger the immune system. The mechanism of action of antibiotics, generally against the cell wall, trying to break "defense" to achieve the destruction of the bacteria.
Researchers have done is an antibiotic administered first, breaking the cell wall of E. coli, it changes shape. Followed by administration of another antibiotic, called for MreB protein, so even if the proliferation of bacteria, it can not return to its original shape, no longer have the ability to infect and eventually die a natural death. They concluded, Rat Progesterone ELISA Kit http://www.cusabio.com/ELISA-Kit/Rat-ProgesteronePROG-ELISA-kit-98271.html is the key to "stealth" in.
Assistant professor of bioengineering at Stanford University, Huang Zhen, said the study could explain the causes of bacterial resistance, "the process of building a better understanding of the cell wall, is expected to contribute to a better antibiotic use strategic planning."

Best Diagnostic Immune Serum

CUSABIO specialize in produces of diagnostic immune serum. Diagnostic Immune Serum used in the prevention and treatment of infectious diseases in animals are obtained from animals that have been immunized with chemically treated antigens. Such serums include antianthrax serum, Aujeszky’s disease serum, swine erysipelas serum, lamb dysenteric serum, trivalent serum against hemorrhagic septicemia, and antitoxic serums against salmonellosis and colibacillosis. CUSABIO use diagnostic immune serums to identify the causative agents of such infectious diseases of animals as anthrax, brucellosis, salmonellosis, listeriosis, and leptospirosis.

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Studies of influenza vaccine to achieve new breakthroughs

ZHOU Dong-ming Shanghai Pasteur Institute research group has made breakthroughs in the field of influenza vaccine research, related research recently published online in "gene therapy", which studies have shown that targeting conserved influenza miRNA fragments can be used as a new means of prevention and control of influenza .

Influenza viruses can infect including human, avian and other hosts. According to statistics, every year about 3 million to 5 million patients with severe influenza, which killed up to 500,000. Flu viruses spread rapidly, widespread, virulent, pose a serious threat to human health, is one of the world's most serious public health problems. Because the influenza virus mutates rapidly, developing new, efficient, universal flu vaccine flu become a hot research field.

Under the guidance of ZHOU Dong-ming, Shanghai Pasteur Institute anti-infection immunity and vaccine research group Zhang Hongbo postdoctoral, doctoral Tang Xin Ying et al., Screened 7 against influenza NP conserved genes and cells through software design, Recombinant mouse Beta-defensin 14 http://www.cusabio.com/Recombinant-Protein/Recombinant-mouse-Beta-defensin-14-11030925.html and has Efficient antagonistic miRNA, miRNA cloning they screened to replication-defective AdC68 E1 region expression, access to seven different influenza-specific miRNA expression of adenovirus.

Researchers in 1011vp AdC68-amiRNA immunized mice against homologous H1N1 influenza infection have 100% protective effect, for heterologous H5N1 and H9N2 as well as some protective effect (40% to 100%).

Antibacterial infection target validation study was progression

Olaf Schneewind Research Group, University of Chicago study found that long-term, the biological function of GGT SrtA of Gram-positive bacteria infection is critical, and from a biological point of view is confirmed by SrtA promising candidate antibacterial targets. Young Choi wide task force to carry out synthetic drugs, improve the activity of small molecules and the physical and chemical properties, and through cross vitro biochemical experiments confirmed that the small molecule inhibition of substrate peptides targeting SrtA and turn peptide reactive surface proteins. Olaf Schneewind Task Force will reveal small molecule peptide Mouse RARRES2 ELISA Kit http://www.cusabio.com/ELISA-Kit/Mouse-Retinoic-acid-receptor-responder-protein-2RARRES2-ELISA-kit-99837.html turn inhibitory activity. Shanghai drug researchers then demonstrated on live bacterial mode of action and regulation of biological phenotype of small molecule inhibitors.

Experiments show that this small molecule can better prolong survival of mice infected with a certain healing effect. The researchers further revealed that the small molecule to inhibit the activity of a broad spectrum of Gram-positive bacteria SrtA, and has further developed into a broad-spectrum treatment-positive infections of new types of antibiotics value and potential.

Experts said the study is further targeting other virulence regulatory targets, the development of efficient activity of specific small molecule candidate compounds validate concepts and provides a technology platform.

The possibility of Nogo receptor-1 inhibition of neurite outgrowth verification

Axons glial cell-derived growth inhibitory protein may limit the adult central nervous system functional repair after injury. Nogo protein, myelin-associated glycoprotein, myelin oligodendrocyte glycoprotein and B lymphocyte stimulator, which usually have four kinds inhibitor Nogo receptor-1 receptor neurons interact to inhibit axonal growth .

Professor Kohtaro Takei Yokohama City University confirmed the lateral olfactory tract guidance material (LOTUS) combined NgR1, would prevent four kinds NgR1 ligand binding, thus weakening NgR1 ligand-induced inhibition of neurite outgrowth. LOTUS neurons Recombinant human DCN1-like protein 1  http://www.cusabio.com/Recombinant-Protein/Recombinant-human-DCN1-like-protein-1-11031298.html have the ability to overcome NgR1-mediated inhibition of axonal growth in the future, LOTUS might be to promote effective NgR1 endogenous inhibitor of neuronal regeneration.

New test measures deadly protein in spinal fluid

The international team of scientists from University College London, IRBM Promidis, University of British Columbia, and CHDI Foundation developed a new ultra-sensitive test using the Singulex SMC Technology Erenna Immunoassay system that is able to detect mutant huntingtin in the cerebrospinal fluid (CSF) of HD patients, including some who carry the HD mutation but have not yet developed symptoms. The test, called a 'single molecule counting assay', combines fluorescent antibodies with Polyclonal Antibody Service http://about.cusabio.com/m-200.html to count individual molecules of mutant huntingtin with a very low detection threshold. The research team's findings were validated in CSF samples from two different groups of volunteers in London and Vancouver.
CSF is a clear fluid produced by the brain that can be collected relatively easily with a needle, through a process known as a lumbar puncture or spinal tap. CSF is used in the diagnosis of other neurodegenerative diseases like Alzheimer's and Parkinson's, but until now the protein that causes HD had never been detected in CSF.
"We think the mutant huntingtin is being released into the CSF from the very brain cells it is killing," said Dr Edward Wild of UCL Institute of Neurology. "It may be a smoking gun that reflects the harm the protein is doing in the living human nervous system."
As well as detecting the protein for the first time, the researchers found that the level of mutant huntingtin was higher in volunteers with more advanced disease. What's more, the concentration of mutant huntingtin predicted the severity of movement and cognitive problems in patients.
"We do not yet have treatments that can slow the progression of Huntington's disease but, when we do, measuring the mutant protein in CSF could guide clinical decisions such as the best time to start a treatment," said Dr Douglas Macdonald at CHDI. "Measuring the amount of huntingtin may also be an essential biomarker for the upcoming trials of huntingtin-lowering therapeutics."
2015 will see the start of the first human clinical trial of a gene silencing or huntingtin-lowering drug, which specifically aims to reduce production of mutant huntingtin in the brains of HD patients. Being able to detect and measure the amount of mutant huntingtin present in the nervous system will be a valuable way of seeing whether the gene-silencing drug is hitting its target and has the intended effect, lowering the amount of disease causing mHTT protein. Meanwhile, this new technique will be an invaluable tool to help researchers study the effects of this devastating disease in the living nervous system.

An accurate screening method for Down

Recently, the University of California, San Francisco (UCSF) researchers have proposed a new method, between 10-14 weeks of pregnancy blood test, a comparable standard non-invasive screening techniques to more effectively diagnose Down syndrome and the other two less common chromosomal abnormalities. The study followed nearly 16,000 pregnant women, pregnancy outcomes, using cell-free DNA blood test correctly identified all fetuses with Down's syndrome (38), Down syndrome is a cognitive disorder associated with disease, increase the risk of several diseases. Researchers by neonatal screening, prenatal or postnatal genetic analysis confirmed these diagnostic results. The present study focuses on the float in maternal blood fraction of fetal DNA. With a molecular "Copy" technique (known as polymerase chain reaction) amplification of DNA and sequenced, so that the relative amount of DNA can be compared between each chromosome.

When the same acceptance criteria for screening pregnant women, the 38 fetuses among them 30 are marked with Down syndrome. Including blood screening for chromosomal defects related hormones and proteins were identified, along with the back of the neck in neck pleated ultrasonic liquid, if one has Down syndrome implies excessive. The average age of the pregnant woman is 30 years old, about a quarter more than 35 years of age, these women have traditionally been considered to have a high risk and invasive prenatal testing for them, such as amniocentesis. The incidence of Down syndrome misdiagnosis relatively low. The standard screening method is recognized can lead to a lot of false positives, the use of cell-free DNA tool is much less false positives. With this new method only have nine false positives, but with 854 times the standard screening rule of false positives. Meanwhile, the researchers found the Recombinant human Apolipoprotein C-III http://www.cusabio.com/Recombinant-Protein/Recombinant-human-Apolipoprotein-C-III-11030819.html in the study population, no DNA screening accuracy is still more than the other standard screening methods. In 10 cases of trisomy 18 (also known as Edwards syndrome), a cell-free DNA techniques to determine the nine cases, there is a false positive. Using standard screening methods were identified eight cases, there are 49 false positives. For Trisomy 13 (also known as trisomy), cell-free DNA testing to identify the two cases, and mark a false positive, while the standard screening method identified only one case, marking 28 false positives.

Although these findings suggest that cell-free DNA screening is superior to standard procedures, but the study highlights the need to pay attention. "Standard Filter" to determine a wide range of abnormal cell-free DNA detection screening for less. Down syndrome cases including more than 50 percent of aneuploidy (abnormal number of chromosomes caused by). Furthermore, there is an unusually high number of aneuploidy in 488 pregnant women, their plasma samples failed because of an insufficient number of fetal DNA contained or incalculable, or sequencing to detect failure or high variance, which will lead to the results difficult to interpret . Approximately 2.7% of these fetuses fetal chromosomal abnormalities, including those with abnormal cell-free DNA techniques have not been found. This is significantly higher than the overall prevalence of 0.4 group. Because the study included the failure queue, the detection rate of cell-free DNA screening tools are low.