TIM-3 Antibody [F19D23] | Primary Antibodies

Application: Reactivity: Mouse

Usage Information

Dilution
WB1:1000 IP1:100 IHC1:200

Application
WB, IP, IHC

Reactivity
Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
45-80 kDa

Datasheet & SDS

Biological Description

Specificity
TIM-3 Antibody [F19D23] detects endogenous levels of total TIM-3 protein.

Clone
F19D23

Synonym(s)
Hepatitis A virus cellular receptor 2 homolog; HAVcr-2; TIMD-3; T-cell immunoglobulin mucin receptor 3 (TIM-3); T-cell membrane protein 3; CD366; Havcr2; Tim3; Timd3

Background
TIM-3 (T cell immunoglobulin and mucin-domain containing-3), encoded by HAVCR2, belongs to the TIM family of transmembrane glycoproteins characterized by an N-terminal immunoglobulin variable (IgV) domain with a unique metal-ion dependent ligand (MID-like) binding site framed by FG and CC′ loops, a glycosylated mucin stalk, a transmembrane domain, and a cytoplasmic tail with five conserved tyrosine residues (e.g., Tyr256 and Tyr263) lacking classical inhibitory motifs but enabling interactions with BAT3, FYN, and LCK. Primarily expressed on activated IFN-γ-producing Th1 and CD8+ T cells, TIM-3 acts as a key inhibitory receptor, where ligand binding (galectin-9 to N-glycans on IgV, phosphatidylserine or CEACAM1 to the FG/CC′ pocket) triggers ITK-mediated phosphorylation of cytoplasmic tyrosines, releasing BAT3 to suppress TCR signaling, promote FYN recruitment for T cell anergy, disrupt immunological synapses via CD45/CD148 association, and induce apoptosis, thereby downregulating Th1 responses, enhancing Treg suppression, and limiting autoimmunity while exacerbating exhaustion in chronic infections and cancer. In myeloid cells like DCs and macrophages, TIM-3 binds HMGB1 or PtdSer to dampen TLR-mediated innate immunity (e.g., nucleic acid sensing), promote apoptotic cell phagocytosis for cross-presentation or tolerance, and inhibit proinflammatory cytokines, contributing to tumor immunosuppression. TIM-3 marks terminally exhausted PD-1+ T cells in tumors/viral infections, drives LSC self-renewal in AML via autocrine galectin-9/β-catenin/mTOR/HIF1α pathways, correlates with poor prognosis, and its blockade synergizes with PD-1 inhibition to restore antitumor immunity. Loss-of-function HAVCR2 mutations impair TIM-3 folding/surface expression, causing hyperinflammation and subcutaneous panniculitis-like T-cell lymphoma.

Background

TIM-3 (T cell immunoglobulin and mucin-domain containing-3), encoded by HAVCR2, belongs to the TIM family of transmembrane glycoproteins characterized by an N-terminal immunoglobulin variable (IgV) domain with a unique metal-ion dependent ligand (MID-like) binding site framed by FG and CC′ loops, a glycosylated mucin stalk, a transmembrane domain, and a cytoplasmic tail with five conserved tyrosine residues (e.g., Tyr256 and Tyr263) lacking classical inhibitory motifs but enabling interactions with BAT3, FYN, and LCK. Primarily expressed on activated IFN-γ-producing Th1 and CD8+ T cells, TIM-3 acts as a key inhibitory receptor, where ligand binding (galectin-9 to N-glycans on IgV, phosphatidylserine or CEACAM1 to the FG/CC′ pocket) triggers ITK-mediated phosphorylation of cytoplasmic tyrosines, releasing BAT3 to suppress TCR signaling, promote FYN recruitment for T cell anergy, disrupt immunological synapses via CD45/CD148 association, and induce apoptosis, thereby downregulating Th1 responses, enhancing Treg suppression, and limiting autoimmunity while exacerbating exhaustion in chronic infections and cancer. In myeloid cells like DCs and macrophages, TIM-3 binds HMGB1 or PtdSer to dampen TLR-mediated innate immunity (e.g., nucleic acid sensing), promote apoptotic cell phagocytosis for cross-presentation or tolerance, and inhibit proinflammatory cytokines, contributing to tumor immunosuppression. TIM-3 marks terminally exhausted PD-1+ T cells in tumors/viral infections, drives LSC self-renewal in AML via autocrine galectin-9/β-catenin/mTOR/HIF1α pathways, correlates with poor prognosis, and its blockade synergizes with PD-1 inhibition to restore antitumor immunity. Loss-of-function HAVCR2 mutations impair TIM-3 folding/surface expression, causing hyperinflammation and subcutaneous panniculitis-like T-cell lymphoma.

References
https://pubmed.ncbi.nlm.nih.gov/33931442/ https://pubmed.ncbi.nlm.nih.gov/34159709/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%