Human Recombinant HAVCR2 - Strep Tagged
Reference ID:KB-3862
Western Blot
Flow Cytometry
Gene of Interest
Gene Synonyms:HAVCR2;TIM3;TIMD3
Protein Names:Hepatitis A virus cellular receptor 2 (HAVcr-2) (T-cell immunoglobulin and mucin domain-containing protein 3) (TIMD-3) (T-cell immunoglobulin mucin receptor 3) (TIM-3) (T-cell membrane protein 3) (CD antigen CD366)
Accession Data
Organism:Homo sapiens (Human)
Mass (kDa):333.94
Length (aa):301
Proteomics (Proteome ID):UP000005640
Proteomics (Chromosome): Chromosome 5
Binding Site:BINDING 111 111 Phosphatidylserine. {ECO:0000250|UniProtKB:Q8VIM0}.; BINDING 118 118 Phosphatidylserine; via amide nitrogen. {ECO:0000250|UniProtKB:Q8VIM0}.
Function [CC]: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 (PubMed:24825777). Regulates macrophage activation (PubMed:11823861). Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance (PubMed:14556005). 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 (PubMed:24337741, PubMed:26492563). In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN (By similarity). Expressed on Treg cells can inhibit Th17 cell responses (PubMed:24838857). Receptor for LGALS9 (PubMed:16286920, PubMed:24337741). Binding to LGALS9 is believed to result in suppression of T-cell responses; the resulting apoptosis of antigen-specific cells may implicate HAVCR2 phosphorylation and disruption of its association with BAG6. Binding to LGALS9 is proposed to be involved in innate immune response to intracellular pathogens. Expressed on Th1 cells interacts with LGALS9 expressed on Mycobacterium tuberculosis-infected macrophages to stimulate antibactericidal activity including IL-1 beta secretion and to restrict intracellular bacterial growth (By similarity). However, the function as receptor for LGALS9 has been challenged (PubMed:23555261). Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes (By similarity). Receptor for phosphatidylserine (PtSer); PtSer-binding is calcium-dependent. May recognize PtSer on apoptotic cells leading to their phagocytosis. Mediates the engulfment of apoptotic cells by dendritic cells. Expressed on T-cells, promotes conjugation but not engulfment of apoptotic cells. Expressed on dendritic cells (DCs) positively regulates innate immune response and in synergy with Toll-like receptors promotes secretion of TNF-alpha. In tumor-imfiltrating DCs suppresses nucleic acid-mediated innate immune repsonse by interaction with HMGB1 and interfering with nucleic acid-sensing and trafficking of nucleid acids to endosomes (By similarity). Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9 (PubMed:22323453). In contrast, shown to suppress NK cell-mediated cytotoxicity (PubMed:22383801). Negatively regulates NK cell function in LPS-induced endotoxic shock (By similarity). {ECO:0000250|UniProtKB:Q8VIM0, ECO:0000269|PubMed:11823861, ECO:0000269|PubMed:14556005, ECO:0000269|PubMed:16286920, ECO:0000269|PubMed:22323453, ECO:0000269|PubMed:23555261, ECO:0000269|PubMed:24838857, ECO:0000269|PubMed:26492563, ECO:0000305|PubMed:24825777}.
Metal Binding:METAL 116 116 Calcium; via carbonyl oxygen. {ECO:0000250|UniProtKB:Q8VIM0}.; METAL 119 119 Calcium. {ECO:0000250|UniProtKB:Q8VIM0}.
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. {ECO:0000269|PubMed:11823861, ECO:0000269|PubMed:17069754, ECO:0000269|PubMed:18006747, ECO:0000269|PubMed:19001139, ECO:0000269|PubMed:19587053, ECO:0000269|PubMed:22323453, ECO:0000269|PubMed:22383801, ECO:0000269|PubMed:24838857}.
Disease:Note=May be involved in T-cell exhaustion associated with chronic viral infections such as with human immunodeficiency virus (HIV) and hepatitic C virus (HCV). {ECO:0000269|PubMed:19001139, ECO:0000269|PubMed:19587053}.
Mutagenesis:MUTAGEN 265 265 Y->A: Abolishes TCR-induced NFAT activation; when associated with A-272. {ECO:0000269|PubMed:26492563}.; MUTAGEN 265 265 Y->E: No effect on TCR-induced NFAT activation (phosphomimetic mutation); when associated with E-272. {ECO:0000269|PubMed:26492563}.; MUTAGEN 272 272 Y->A: Abolishes TCR-induced NFAT activation; when associated with A-265. {ECO:0000269|PubMed:26492563}.; MUTAGEN 272 272 Y->E: No effect on TCR-induced NFAT activation (phosphomimetic mutation); when associated with E-265. {ECO:0000269|PubMed:26492563}.
Reagent Data
Class:Immune Checkpoint
Region:Ser 22 - Arg 200
Molecular Weight:22.9
Purification System:Chromatography
Formulation:Sterile-filtered colorless solution
Formulation Concentration:1 mg/ml
Buffer Volume:Standard
Buffer Solution:PBS
Endotoxin Level:< 1%
Aggregate Tested By:SDS-PAGE
Endotoxin Screened:< 0.1 ng/ug
Purity:> 98%
Determined: SDS-PAGE
Validated: RP-HPLC
Sample Handling
Stability:This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:Reconstitute in sterile distilled H2O to no less than 100 ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.