protein

Fc gamma RIIIA/CD16a Protein, Human (F176V, HEK293, SUMO-His)

HY-P78676

5 μg;10 μg;50 μg;100 μg;500 μg;1 mg

38;62;162;260;680;1100 USD

Fc gamma RIIIA/CD16a Protein, Human (F176V, HEK293, SUMO-His)

proteins

HEK293

5 μg;10 μg;50 μg;100 μg;500 μg;1 mg

38;62;162;260;680;1100 USD

Fc gamma RIIIA/CD16a protein is a receptor for the Fc fragment of IgG and activates antibody-dependent cellular cytotoxicity (ADCC) upon binding to antigen-IgG complexes. It mediates IgG effector functions on NK cells, generating memory-like adaptive NK cells to efficiently eliminate virally infected cells. Fc gamma RIIIA/CD16a Protein, Human (F176V, HEK293, SUMO-His) is the recombinant human-derived Fc gamma RIIIA/CD16a protein, expressed by HEK293 , with C-His, N-SUMO labeled tag and F176V, , , , mutation. The total length of Fc gamma RIIIA/CD16a Protein, Human (F176V, HEK293, SUMO-His) is 192 a.a., with molecular weight of 42-65 kDa.

Human

Fc gamma RIIIA/CD16a Protein serves as a receptor for the invariable Fc fragment of immunoglobulin gamma (IgG), optimally activated upon binding clustered antigen-IgG complexes displayed on cell surfaces, initiating antibody-dependent cellular cytotoxicity (ADCC). This process involves the lysis of antibody-coated cells, preventing inappropriate effector cell activation in the absence of an antigenic trigger. The protein mediates IgG effector functions on natural killer (NK) cells, binding antigen-IgG complexes generated during infection to trigger NK cell-dependent cytokine production and degranulation. Fc gamma RIIIA/CD16a is crucial in generating memory-like adaptive NK cells that efficiently eliminate virus-infected cells via ADCC. It regulates NK cell survival, proliferation, and prevents NK cell progenitor apoptosis. As an Fc-binding subunit, it associates with CD247 and/or FCER1G adapters to form functional signaling complexes, leading to intracellular signaling cascades that drive NK cell activation. The protein also plays a role in mediating the antitumor activities of therapeutic antibodies, triggering TNFA-dependent ADCC of IgG-coated tumor cells and enhancing ADCC in response to afucosylated IgGs. In the context of Dengue virus infection, Fc gamma RIIIA/CD16a is involved in pathogenesis through an antibody-dependent enhancement (ADE) mechanism, facilitating virus entry into myeloid cells and subsequent viral replication during secondary infections.

FCGR3A; CD16A; FCG3; FCGR3; IGFR3

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized a 0.22 μm filtered solution of 20 mM PB, 150 mM NaCl, pH 7.4.

Room temperature in continental US; may vary elsewhere.