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  • 产品名称：Human CD16a (FcgR3a) protein (Recombinant) {Biotin} (STJP000193)

  • 产品型号：STJP000193
  • 产品厂商：ST john's laboratory
  • 产品文档：
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简单介绍：
Human CD16a (FcgR3a) protein (Recombinant) {Biotin} (STJP000193)
详情介绍：
Host: HEK293
Applications: ELISA/WB
Note: STRICTLY FOR FURTHER RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Recombinant-Human CD16a (FcgR3a)-protein was developed from hek293. For use in research applications.
Conjugation: Biotin
Formulation: 0.2 Mu m filtered PBS solution, pH7.2.
Dilution Range: A quick spin of the vial followed by reconstitution in distilled water to a concentration not less than 0.1 mg/mL.
Storage Instruction: Can be stored in working aliquots at 2°C-8°C C for one month, or at-20°C to-70°C for 1 year. Avoid repeated freeze/thaw cycles. NA
Endotoxin: Endotoxin content was assayed using a LAL gel clot method. Endotoxin level was found to be less than 0.1 ng/µg (1EU/µg). NA
Gene Symbol: FCGR3A
Gene ID: 2214
Uniprot ID: FCG3A_HUMAN
Immunogen Region: ECD
Immunogen: Optimized DNA sequence encoding Human extracellular domain of human CD16aincluding a C-terminal 6His tag was expressed in HEK293 cells. CD16a was further labled by Biotin for detection by avidin conjugated secondary probes. NA
Tissue Specificity Expressed in natural killer cells (at protein level). Expressed in a subset of circulating monocytes (at protein level).
Post Translational Modifications Glycosylated. Contains high mannose- and complex-type oligosaccharides. Glycosylation at Asn-180 is mandatory for high affinity binding to the Fc and for discrimination between fucosylated and afucosylated IgG glycoforms. Undergoes rapid ectodomain shedding upon NK cell stimulation. The soluble form is produced by a proteolytic cleavage mediated by ADAM17. Repeated stimulation causes receptor shedding, a mechanism that allows for increased NK cell motility and detachment from opsonized target cells while avoiding activation-induced NK cell apoptosis. Phosphorylated at RSSTR motif by PKC. The relevant physiological PKCs might be PRKCI, PRKCG, PRKCE, PRKCH and PRKCQ.
Function Receptor for the invariable Fc fragment of immunoglobulin gamma (IgG). Optimally activated upon binding of clustered antigen-IgG complexes displayed on cell surfaces, triggers lysis of antibody-coated cells, a process known as antibody-dependent cellular cytotoxicity (ADCC). Does not bind free monomeric IgG, thus avoiding inappropriate effector cell activation in the absence of antigenic trigger. Mediates IgG effector functions on natural killer (NK) cells. Binds antigen-IgG complexes generated upon infection and triggers NK cell-dependent cytokine production and degranulation to limit viral load and propagation. Involved in the generation of memory-like adaptive NK cells capable to produce high amounts of IFNG and to efficiently eliminate virus-infected cells via ADCC. Regulates NK cell survival and proliferation, in particular by preventing NK cell progenitor apoptosis. Fc-binding subunit that associates with CD247 and/or FCER1G adapters to form functional signaling complexes. Following the engagement of antigen-IgG complexes, triggers phosphorylation of immunoreceptor tyrosine-based activation motif (ITAM)-containing adapters with subsequent activation of phosphatidylinositol 3-kinase signaling and sustained elevation of intracellular calcium that ultimately drive NK cell activation. The ITAM-dependent signaling coupled to receptor phosphorylation by PKC mediates robust intracellular calcium flux that leads to production of pro-inflammatory cytokines, whereas in the absence of receptor phosphorylation it mainly activates phosphatidylinositol 3-kinase signaling leading to cell degranulation. Costimulates NK cells and trigger lysis of target cells independently of IgG binding. Mediates the antitumor activities of therapeutic antibodies. Upon ligation on monocytes triggers TNFA-dependent ADCC of IgG-coated tumor cells. Mediates enhanced ADCC in response to afucosylated IgGs. (Microbial infection) Involved in Dengue virus pathogenesis via antibody-dependent enhancement (ADE) mechanism. Secondary infection with Dengue virus triggers elevated levels of afucosylated non-neutralizing IgG1s with reactivity to viral envelope/E protein. Viral antigen-IgG1 complexes bind with high affinity to FCGR3A, facilitating virus entry in myeloid cells and subsequent viral replication.
Protein Name Low Affinity Immunoglobulin Gamma Fc Region Receptor Iii-A
Igg Fc Receptor Iii-A
Cd16-Ii
Cd16a Antigen
Fc-Gamma Riii-Alpha
Fc-Gamma Riii
Fc-Gamma Riiia
Fcriii
Fcriiia
Fcgammariiia
Fcr-10
Igg Fc Receptor Iii-2
Cd Antigen Cd16a
Database Links Reactome: R-HSA-198933
Reactome: R-HSA-2029481
Reactome: R-HSA-2029482
Reactome: R-HSA-2029485
Reactome: R-HSA-9664323
Reactome: R-HSA-9664422
Cellular Localisation Cell Membrane
Single-Pass Type I Membrane Protein
Secreted
Exists Also As A Soluble Receptor
Alternative Protein Names Low Affinity Immunoglobulin Gamma Fc Region Receptor Iii-A protein
Igg Fc Receptor Iii-A protein
Cd16-Ii protein
Cd16a Antigen protein
Fc-Gamma Riii-Alpha protein
Fc-Gamma Riii protein
Fc-Gamma Riiia protein
Fcriii protein
Fcriiia protein
Fcgammariiia protein
Fcr-10 protein
Igg Fc Receptor Iii-2 protein
Cd Antigen Cd16a protein
FCGR3A protein
CD16A protein
FCG3 protein
FCGR3 protein
IGFR3 protein

Information sourced from Uniprot.org

12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance
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