Anti-TIM 1/HAVCR1 Antibody Picoband® Fluoro647 Conjugated

KIM1 (KIDNEY INJURY MOLECULE 1), also known as HAVCR1, HAVCR or TIM1, is a protein that in humans is encoded by the KIM1 gene. The KIM1 gene is mapped to 5q33.3. Biochemical, mutational, and cell adhesion analyses confirm that Tim1 is capable of homophilic Tim-Tim interactions. The features identified in murine KIM1 is conserved in human KIM1. The KIM1 protein is indeed a receptor for the virus through the infection of canine osteogenic sarcoma cells expressing HAVCR1 with HAV. Using a monoclonal antibody to mouse Tim1, Tim1 is expressed after activation of naive T cells and on T cells differentiated in Th2-polarizing conditions. Ectopic expression of KIM1 during mouse T-cell differentiation leads to production of the Th2-type cytokine Il4, but not the Th1-type cytokine Ifng. KIM1-expressing epithelial cells internalized apoptotic bodies, and Kim1 is ly responsible for phagocytosis in cultured primary rat tubule epithelial cells and in porcine and canine epithelial cell lines.

Hepatitis A virus cellular receptor 1 homolog; HAVcr-1; Kidney injury molecule 1; KIM-1; T cell immunoglobulin and mucin domain-containing protein 1; TIMD-1; Havcr1; Kim1

Expressed at a low level in normal kidney but are increased dramatically in postischemic kidney. Expressed in proliferating bromodeoxyuridine-positive and dedifferentiated vimentin-positive epithelial cells in regenerating proximal tubules. .

May play a role in T-helper cell development and the regulation of asthma and allergic diseases. Receptor for TIMD4. May play a role in kidney injury and repair (By similarity) . .

1. de Souza, A. J., Oriss, T. B., O'Malley, K. J., Ray, A., Kane, L. P. T cell Ig and mucin 1 (TIM-1) is expressed on in vivo-activated T cells and provides a costimulatory signal for T cell activation. Proc. Nat. Acad. Sci. 102: 17113-17118, 2005. 2. Feigelstock, D., Thompson, P., Mattoo, P., Zhang, Y., Kaplan, G. G. The human homolog of HAVcr-1 codes for a hepatitis A virus cellular receptor. J. Virol. 72: 6621-6628, 1998.