FCGR2B

The protein encoded by this gene is a low affinity receptor for the Fc region of immunoglobulin gamma complexes. The encoded protein is involved in the phagocytosis of immune complexes and in the regulation of antibody production by B-cells. Variations in this gene may increase susceptibilty to systemic lupus erythematosus (SLE). Several transcript variants encoding different isoforms have been found for this gene.

Fc receptor, IgG, low affinity Iib

Receptor for the Fc region of complexed or aggregated immunoglobulins gamma. Low affinity receptor. Involved in a variety of effector and regulatory functions such as phagocytosis of immune complexes and modulation of antibody production by B-cells. Binding to this receptor results in down-modulation of previous state of cell activation triggered via antigen receptors on B-cells (BCR), T-cells (TCR) or via another Fc receptor. Isoform IIB1 fails to mediate endocytosis or phagocytosis. Isoform IIB2 does not trigger phagocytosis.

Antigen processing and presentation of exogenous peptide antigen via MHC class II Source: ARUK-UCL
Cell surface receptor signaling pathway Source: GO_Central
Cellular response to amyloid-beta Source: ARUK-UCL
Cellular response to molecule of bacterial origin Source: ARUK-UCL
Cerebellum development Source: BHF-UCL
Defense response Source: ARUK-UCL
Fc-gamma receptor signaling pathway involved in phagocytosis Source: ARUK-UCL
Follicular B cell differentiation Source: ARUK-UCL
Follicular dendritic cell activation Source: ARUK-UCL
Immune complex clearance by monocytes and macrophages Source: ARUK-UCL
Immune response Source: ProtInc
Immunoglobulin mediated immune response Source: ARUK-UCL
Inflammatory response Source: ARUK-UCL
Mature B cell differentiation involved in immune response Source: ARUK-UCL
Negative regulation of acute inflammatory response to antigenic stimulus Source: ARUK-UCL
Negative regulation of antibody-dependent cellular cytotoxicity Source: ARUK-UCL
Negative regulation of B cell activation Source: ARUK-UCL
Negative regulation of B cell proliferation Source: ARUK-UCL
Negative regulation of B cell receptor signaling pathway Source: ARUK-UCL
Negative regulation of cytokine production Source: ARUK-UCL
Negative regulation of cytotoxic T cell degranulation Source: ARUK-UCL
Negative regulation of dendritic cell antigen processing and presentation Source: ARUK-UCL
Negative regulation of dendritic cell differentiation Source: ARUK-UCL
Negative regulation of humoral immune response mediated by circulating immunoglobulin Source: ARUK-UCL
Negative regulation of immune response Source: ARUK-UCL
Negative regulation of immunoglobulin production Source: ARUK-UCL
Negative regulation of interleukin-10 production Source: ARUK-UCL
Negative regulation of macrophage activation Source: ARUK-UCL
Negative regulation of neutrophil activation Source: ARUK-UCL
Negative regulation of phagocytosis Source: ARUK-UCL
Negative regulation of type I hypersensitivity Source: ARUK-UCL
Phagocytosis, engulfment Source: ARUK-UCL
Positive regulation of humoral immune response Source: ARUK-UCL
Positive regulation of JNK cascade Source: BHF-UCL
Positive regulation of neuron death Source: BHF-UCL
Positive regulation of phagocytosis Source: ARUK-UCL
Positive regulation of response to endoplasmic reticulum stress Source: ARUK-UCL
Receptor-mediated endocytosis Source: ARUK-UCL
Regulation of adaptive immune response Source: ARUK-UCL
Regulation of B cell antigen processing and presentation Source: ARUK-UCL
Regulation of dendritic spine maintenance Source: ARUK-UCL
Regulation of immune complex clearance by monocytes and macrophages Source: ARUK-UCL
Regulation of immune response Source: GO_Central
Regulation of innate immune response Source: ARUK-UCL
Regulation of signaling receptor activity Source: ARUK-UCL
Response to bacterium Source: ARUK-UCL
Signal transduction Source: ProtInc

Cell membrane

Systemic lupus erythematosus (SLE):
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.

Extracellular: 43-217
Helical: 218-240
Cytoplasmic: 241-310

Phosphorylated by the SRC-type Tyr-kinases LYN and BLK.