• Western blot analysis of extracts of various cell lines, using FCGR3A antibody (STJ23643) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (STJS000856) at 1:10000 dilution. Lysates/proteins: 25 Mu g per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit. Exposure time: 3s.

Anti-FCGR3A antibody (150-250) (STJ23643)

SKU:
STJ23643

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Host: Rabbit
Applications: WB
Reactivity: Human/Mouse/Rat
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-FCGR3A (150-250) is suitable for use in Western Blot research applications.
Clonality: Polyclonal
Conjugation: Unconjugated
Isotype: IgG
Formulation: PBS with 0.02% Sodium Azide, 50% Glycerol, pH7.3.
Purification: Affinity purification
Dilution Range: WB 1:500-1:1000
Storage Instruction: Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles.
Gene Symbol: FCGR3A
Gene ID: 2214
Uniprot ID: FCG3A_HUMAN
Immunogen Region: 150-250
Immunogen: A synthetic peptide corresponding to a sequence within amino acids 150-250 of human FCGR3A (NP_000560.7).
Immunogen Sequence: YFHHNSDFYIPKATLKDSGS YFCRGLFGSKNVSSETVNIT ITQGLAVSTISSFFPPGYQV SFCLVMVLLFAVDTGLYFSV KTNIRSSTRDWKDHKFKWRK D
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 Antibody Names Anti-Low Affinity Immunoglobulin Gamma Fc Region Receptor Iii-A antibody
Anti-Igg Fc Receptor Iii-A antibody
Anti-Cd16-Ii antibody
Anti-Cd16a Antigen antibody
Anti-Fc-Gamma Riii-Alpha antibody
Anti-Fc-Gamma Riii antibody
Anti-Fc-Gamma Riiia antibody
Anti-Fcriii antibody
Anti-Fcriiia antibody
Anti-Fcgammariiia antibody
Anti-Fcr-10 antibody
Anti-Igg Fc Receptor Iii-2 antibody
Anti-Cd Antigen Cd16a antibody
Anti-FCGR3A antibody
Anti-CD16A antibody
Anti-FCG3 antibody
Anti-FCGR3 antibody
Anti-IGFR3 antibody

Information sourced from Uniprot.org

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