Mouse TIM-1/KIM-1/HAVCR Antibody Summary
Tyr22-Thr212
Accession # NP_001160104
Applications
This antibody functions as an ELISA detection antibody when paired with Rat Anti-Mouse TIM‑1/KIM‑1/HAVCR Monoclonal Antibody (Catalog # MAB1817).
This product is intended for assay development on various assay platforms requiring antibody pairs. We recommend the Mouse TIM-1/KIM-1/HAVCR DuoSet ELISA Kit (Catalog # DY1817) for convenient development of a sandwich ELISA or the Mouse TIM-1/KIM-1/HAVCR Quantikine ELISA Kit (Catalog # MKM100) for a complete optimized ELISA.
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
Mouse TIM‑1/KIM‑1/HAVCR ELISA Standard Curve. Recombinant Mouse TIM-1/KIM-1/HAVCR protein was serially diluted 2-fold and captured by Rat Anti-Mouse TIM-1/KIM-1/HAVCR Monoclonal Antibody (Catalog # MAB1817) coated on a Clear Polystyrene Microplate (Catalog # DY990). Rat Anti-Mouse TIM-1/KIM-1/HAVCR Monoclonal Antibody (Catalog # MAB18171) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998) followed by Substrate Solution (Catalog # DY999) and stopping the enzymatic reaction with Stop Solution (Catalog # DY994).
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: TIM-1/KIM-1/HAVCR
TIM-1 (T cell-immunoglobulin-mucin; also known as KIM-1 or HAVCR) is a 70-80 kDa, type I transmembrane glycoprotein member of the TIM family of immunoglobulin superfamily molecules (1-4). This gene family is involved in the regulation of Th1 and Th2-cell-mediated immunity. In mouse, there are eight known TIM genes (# 1-8) vs. only three genes in human (# 1, 3, and 4) (1, 2). Mouse TIM-1 and -2 are counterparts of human TIM-1 while mouse TIM-5 through 8 have no human counterparts (2). Mouse TIM-1 is synthesized as a 305 amino acid (aa) precursor that contains a 21 aa signal sequence, a 216 aa extracellular domain (ECD), a 21 aa transmembrane segment and a 47 aa cytoplasmic domain (5, 6). The ECD contains one V-type Ig-like domain and a mucin region characterized by multiple T-S-P motifs. The mucin region undergoes extensive O-linked glycosylation. The mouse TIM-1 gene is highly polymorphic and, based on rat, may undergo alternate splicing (4, 6). For instance, HBA mice show a 15 aa deletion in the mucin region that occurs in BALB/c mice (6). This difference is associated with a decreased susceptibility to asthma. Other polymorphisms are also documented (6). In human, TIM-1 is known to circulate as a soluble form. It undergoes constitutive cleavage by an undefined MMP, releasing a 75-85 kDa soluble molecule (5). The same thing might be expected in mouse. The ECD of mouse TIM-1 is 50%, 39% and 80% aa identical to human, canine and rat TIM-1 ECD, respectively. The only two reported ligands for TIM-1 are TIM-4 and the hepatitis A virus (8, 9). However, others are believed to exist, and based on the ligand for TIM-3, one possibility might be an S-type lectin (10). TIM-1 ligation induces T cell proliferation and promotes cytokine production (1, 10). In particular, it induces IL-4 production, and requires the cytoplasmic tyrosine phosphorylation motif (5).
- Meyers, J.H. et al. (2005) Trends Mol. Med. 11:1471.
- Kuchroo, V.K. et al. (2003) Nat. Rev. Immunol. 3:454.
- Mariat, C. et al. (2005) Phil. Trans. R. Soc. B 360:1681.
- Ichimura, T. et al. (1998) J. Biol. Chem. 273:4135.
- de Souza, A.J. et al. (2005) Proc. Natl. Acad. Sci. USA 102:17113.
- McIntire, J.J. et al. (2001) Nat. Immunol. 2:1109.
- Bailly, V. et al. (2002) J. Biol. Chem. 277:39739.
- Feigelstock, D. et al. (1998) J. Virol. 72:6621.
- Zhu, C. et al. (2005) Nat. Immunol. 6:1245.
- Meyers, J.H. et al. (2005) Nat. Immunol. 6:455.
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