Primary Antibody

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Synaptotagmins constitute a family of membrane trafficking proteins which are characterized by an Nterminal transmembrane region (TMR), a varying linker, and 2 C-terminal C2 domain names – C2A and C2B. There are 15 members in the synaptotagmin family. You will find several comprising protein families which are associated with synaptotagmins, such as transmembrane (Ferlins, E-Syts, and MCTPs) and potassium (RIMs, Munc13s, synaptotagmin-related proteins and B/K) proteins. The synaptotagmins are integral membrane proteins of synaptic vesicles believed to function as Ca(2+) sensors in the process of vesicular trafficking and exocytosis. Magnesium binding to synaptotagmin participates in triggering neurotransmitter release. The C2 domain mediates interaction. Synaptotagmin can have a function in the membrane interactions during trafficking of synaptic vesicles. It binds acidic phospholipids. It may bind to at least three additional proteins in a Ca(2+)-independent way; those are neurexins, syntaxin and AP2 (1, 2). Synaptotagmin-6 is localized to the endoplasmic reticulum perinuclear compartment. It could be significant for calcium and trafficking since it’s especially expressed in cells signaling. SytVI is within the region of spermatozoa. The cytosolic domain of SytVI may abrogate exocytosis by competing with the endogenous protein for key connections with the fusion machines included with a acrosomal exocytosis.

The anti-LPS antibody material of industrial intravenous immunoglobulins was analyzed by quantitative ELISA using LPS preparations from Escherichia coli, Klebsiella and Pseudomonas aeruginosa O serotypes occurring most often in Gram-negative septicaemia. Three IgG products from producers and one merchandise that was IgM-enriched were analyzed. Mean antibody levels were significantly greater at the IgM fraction of their product that is IgM-enriched compared to’pure’ IgG products, indicating that natural antibodies against bacterial LPS belong mostly to the IgM class. Immunoblotting studies showed that antibody specificities were directed against O side chain epitopes. Antibodies against rough mutant LPS representing a variety of chemotypes were detected in IgG but not in IgM products. The absence of antibodies against Vibrio cholerae LPS indicated that human anti-LPS radicals lead to constant environmental exposure to Gram-negative pathogens. These statistics support the development of infections for IgM-enriched trainings for therapy and prophylaxis.

Members of the ZAS family, such as ZAS1 (HIVEP1), are large proteins which contain a ZAS domainname, a modular protein structure composed of a set of C2H2 zinc fingers with an acidic-rich region and a serine/threonine-rich sequence. These proteins bind specific DNA sequences, including the kappa-B theme (GGGACTTTCC), in the promoters and enhancer regions of several genes and viruses, including human immunodeficiency virus (HIV). ZAS genes span more than 150 kb and contain 10 or more exons, one of which is more than 5.5 kb. Synonyms: Monoclonal HIVEP1 antibody, Anti-HIVEP1 antibody, Human immunodeficiency virus type I enhancer binding protein antibody, CIRIP antibody, MBP-1 antibody, ZNF40 antibody, CRYBP1 antibody, PRDII-BF1 antibody.

SHH gene encodes a protein that is instrumental in patterning the early embryo. It has been implicated in patterning of the somites, the limb axis, as well as the neural tube. Of three human proteins demonstrating functional and sequence similarity to the sonic hedgehog protein of Drosophila, this protein is the most similar. The protein is made as a precursor that’s autocatalytically cleaved; while the C-terminal portion is involved in precursor processing, the N-terminal portion is soluble and has the action. To the point, the C-terminal merchandise covalently attaches a cholesterol moiety to the solution, limiting the N-terminal merchandise to the surface and preventing it from diffusing through the growing embryo. Defects in this protein or in its own signalling pathway are a cause of holoprosencephaly (HPE), a disorder where the developing forebrain fails to correctly separate into right and left hemispheres. Facial deformities manifest HPE. It’s also believed that mutations in this gene or in its signalling pathway may be liable for VACTERL syndrome, which is distinguished by vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal dysplasia, cardiac anomalies, and rectal abnormalities. Furthermore, mutations in a long-range enhancer located approximately 1 megabyte upstream of the gene disrupt limb patterning and could result in preaxial polydactyly.

HIF-1 alpha may be challenging goal to utilize so we’ve put together a summary of all of the important information you want to know including helpful tips. This may be seen from the protocols tab alternatively click hereto get the English version and hereto get the Mandarin.
Under conditions that are normoxic HIF-1 alpha has a. It’s mostly undetectable in cells or cells . It’s stabilized at O2 concentrations under 5 percent and upon insertion under conditions, HIF-1 translocates into the nucleus. Hypoxia can be triggered with treatment utilizing specific representatives e.g. CoCl2 or DFO, etc. . appropriate sample preparation is crucial.

Alexa Fluor® conjugates stay fluorescent over a wide pH range and are photostable. The emission and excitation maxima are equal to those of FITC. Alexa Fluor® 488 will be much more ideal and brighter . Because of emission properties and excitation but spillover attributes, FITC and Alexa Fluor® 488 can’t be used. Alexa Fluor® 488 exhibits photostability, making it acceptable for microscopy.

CD156c, also referred to as a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), is a 748 amino acid type I membrane glycoprotein ubiquitously expressed on many cell types. It is made of domains, such as a prodomaindomain, a cysteine-rich domainname, transmembranous domainname, and a cytoplasmic domainnames. It’s called a precursor protein and becomes through taking away the prodomain by proprotein convertase 7 and also fun. ADAM10 acts as metalloproteinase to cleave a number of molecules such as Notch, pro-TNF-α, amyloid precursor protein, myelin basic protein, and type IV collagen. It mediates endothelial transmigration to be regulated by the launch of cell adhesion molecules like vascular endothelial cadherin or even L-selectin. Dysregulation of ADAM action can lead to the pathogenesis of cardiovascular ailments.

Endothelial protein C receptor EPCR, also referred to as CD201, is a 46 kD N-glycosylated type I transmembrane protein, mostly expressed on the endothelial cells of veins and arteries at lung and heart. It’s also expressed at high levels on a subset of cells and a subset of stem cells. CD201 acts as a receptor for protein C activation, also leads to inhibition of intrinsic and extrinsic coagulation pathways. Additionally, it has a significant part such as inflammation reactions to injury, disease, hematopoiesis, and reaction. Deletion of this gene in mice contributes to embryonic lethality 10, signaling that saying that is CD201 is essential for embryo growth. Mutations of all CD201 happen to be correlated with fetal loss and myocardial infarction in addition to with cerebral thromboembolism .

Endothelial protein C receptor EPCR, also referred to as CD201, is a 46 kD N-glycosylated type I transmembrane protein, mostly expressed on the endothelial cells of veins and arteries at lung and heart. It’s also expressed at high levels on a subset of cells and a subset of stem cells. CD201 acts as a receptor for protein C activation, also leads to inhibition of intrinsic and extrinsic coagulation pathways. Additionally, it has a significant part such as inflammation reactions to injury, disease, hematopoiesis, and reaction. Deletion of this gene in mice contributes to embryonic lethality 10, signaling that saying that is CD201 is essential for embryo growth. Mutations of all CD201 happen to be correlated with fetal loss and myocardial infarction in addition to with cerebral thromboembolism .

The exocyst is a protein complex that guarantees spatial of vesicles into the plasma membranes. We provide microarray data acquired from differentiating mouse embryonic stem cell cultures which identify an up-regulation of exocyst complex part 3-like two (exoc3l2) mRNA in blood vessels. Vascular expression of exoc3l2 is supported by qPCR evaluation of different mouse cells and immunofluorescence analyses of mouse brain sections. We discover an up-regulation of electronic xoc3l2 mRNA synthesis in primary human endothelial cells in response to VEGFA, and this reaction is improved when the cells have been grown on a three-dimensional collagen I matrix. Using the protein EXOC4, and detection of EXOC3L2 show partial subcellular colocalization with EXOC7 and EXOC4. Finally, we show that exoc3l2 silencing inhibits VEGF receptor 2 phosphorylation and VEGFA-directed migration of cultured endothelial cells.

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