Tim3 Mouse Monoclonal Antibody [1E3] (EM1701-19)

UNIPROT #

Q8TDQ0

PROTEIN NAME

Tim3

SYNONYMS

CD366 antibody;FLJ14428 antibody;HAVcr-2 antibody;Havcr2 antibody;HAVR2_HUMAN antibody;Hepatitis A virus cellular receptor 2 antibody;Kidney injury molecule 3 antibody;KIM 3 antibody;KIM3 antibody;T cell immunoglobulin and mucin domain containing 3 antibody;T cell immunoglobulin mucin 3 antibody;T-cell immunoglobulin and mucin domain-containing protein 3 antibody;T-cell immunoglobulin mucin family member 3 antibody;T-cell immunoglobulin mucin receptor 3 antibody;T-cell membrane protein 3 antibody;Tim 3 antibody;TIM-3 antibody;TIM3 antibody;TIMD-3 antibody;TIMD3 antibody

SEQUENCE SIMILARITIES

Belongs to the immunoglobulin superfamily. TIM family.

TISSUE SPECIFICITY

Expressed in T-helper type 1 (Th1) lymphocytes. Expressed on regulatory T (Treg) cells after TCR stimulation. Expressed in dendritic cells and natural killer (NK) cells. Expressed in epithelial tissues. Expression is increased on CD4+ and CD8+ T-cells in chronic hepatitis C virus (HCV) infection. In progressive HIV-1 infection, expression is up-regulated on HIV-1-specific CD8 T-cells.

POST-TRANSLATIONAL MODIFICATION

O-glycosylated with core 1 or possibly core 8 glycans.; Phosphorylated on tyrosine residues; modestly increased after TCR/CD28 stimulation. Can be phosphorylated in the cytoplasmatic domain by FYN (By similarity). Phosphorylation at Tyr-265 is increased by stimulation with ligand LGALS9.

SUBCELLULAR LOCATION

Membrane. Cell junction.

FUNCTION

Cell surface receptor implicated in modulating innate and adaptive immune responses. Generally accepted to have an inhibiting function. Reports on stimulating functions suggest that the activity may be influenced by the cellular context and/or the respective ligand. Regulates macrophage activation. Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance. In CD8+ cells attenuates TCR-induced signaling, specifically by blocking NF-kappaB and NFAT promoter activities resulting in the loss of IL-2 secretion. The function may implicate its association with LCK proposed to impair phosphorylation of TCR subunits, and/or LGALS9-dependent recruitment of PTPRC to the immunological synapse.