TIM3 anticorps (C-Term)
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- Antigène Voir toutes TIM3 (TIM 3) Anticorps
- TIM3 (TIM 3) (Hepatitis A Virus Cellular Receptor 2 (TIM 3))
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Épitope
- C-Term
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Reactivité
- Humain, Rat
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Hôte
- Lapin
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Clonalité
- Polyclonal
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Conjugué
- Cet anticorp TIM3 est non-conjugé
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Application
- Western Blotting (WB), ELISA, Immunohistochemistry (IHC)
- Specificité
- HAVCR2 Antibody detects endogenous levels of total HAVCR2.
- Homologie
- Horse,Dog
- Purification
- The antiserum was purified by peptide affinity chromatography using SulfoLinkTM Coupling Resin (Thermo Fisher Scientific).
- Immunogène
- A synthesized peptide derived from human HAVCR2, corresponding to a region within C-terminal amino acids.
- Isotype
- IgG
- Top Product
- Discover our top product TIM 3 Anticorps primaire
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- Indications d'application
- WB 1:500-1:2000, IHC 1:50-1:200, ELISA(peptide) 1:20000-1:40000
- Restrictions
- For Research Use only
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- Format
- Liquid
- Concentration
- 1 mg/mL
- Buffer
- Rabbit IgG in phosphate buffered saline , pH 7.4, 150 mM NaCl, 0.02 % sodium azide and 50 % glycerol.
- Agent conservateur
- Sodium azide
- Précaution d'utilisation
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- Stock
- -20 °C
- Stockage commentaire
- Store at -20 °C. Stable for 12 months from date of receipt.
- Date de péremption
- 12 months
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- Antigène
- TIM3 (TIM 3) (Hepatitis A Virus Cellular Receptor 2 (TIM 3))
- Autre désignation
- HAVCR2 (TIM 3 Produits)
- Synonymes
- anticorps HAVCR2, anticorps MGC140131, anticorps HAVcr-2, anticorps KIM-3, anticorps TIM3, anticorps TIMD-3, anticorps TIMD3, anticorps Tim-3, anticorps TIM-3, anticorps Tim3, anticorps Timd3, anticorps tim3, anticorps hepatitis A virus cellular receptor 2, anticorps HAVCR2, anticorps Havcr2
- Classe de substances
- Virus
- Sujet
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Description: 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).
Gene: HAVCR2
- Poids moléculaire
- 33kDa
- ID gène
- 84868
- UniProt
- Q8TDQ0
- Pathways
- Regulation of Lipid Metabolism by PPARalpha, Cancer Immune Checkpoints
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