SCUBA

IGSF8 — Immunoglobulin superfamily member 8

IGSF8 belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

IGSF8's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsLymphocyte Homeostatic Regulation
Housekeeping
BSG, CTDSP1, FBXW5, HMGN4, IKBKG, LRP10, MFNG, RASAL3 +8 more

About the gene

SynonymsCD316, CD81P3, EWI2, PGRL
Chromosome1: 160091340-160098943
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classCD markers, Predicted intracellular proteins, Predicted membrane proteins
Molecular functionReceptor

Function

Member of the immunoglobulin superfamily (IgSF) that links tetraspanin-enriched microdomains to the actin cytoskeleton and plays several important roles in innate and adaptive immunity. Acts as an inducible receptor of HSPA8 on dendritic cells to enhance the CCL21/SLC-dependent migration of activated mature dendritic cells while attenuating their antigen- specific stimulatory capacities. In complex with alpha-actinins ACTN1 and ACTN4, regulates actin dynamics in the immune synapse and subsequent T-cell activation. Inhibits the entry of several viruses such as hepatitis C Virus (HCV) or HIV-1. Mechanistically, promotes a change in CD81 organization at the plasma membrane by significantly restricting its diffusion which in turn influences CD81 interaction with Claudin-1/CLDN1, preventing CLDN1 from acting as a co-receptor required for HCV entry. Accumulates at the presynaptic terminal, the producer cell side of the virological synapse, to prevent HIV-1 Env-mediated cell-cell fusion. Highly expressed on malignant cells with antigen presentation defects, interacts with NK receptor KIR3DL2 to suppress NK-cell cytotoxicity. May participate in the regulation of neurite outgrowth and maintenance of the neural network in the adult brain.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.