Biotinylated Human TIM-3 / HAVCR2 Protein, Avitag™,His Tag

Source : 

Biotinylated Human TIM-3, Avitag,His Tag (TM3-H82E7) is expressed from human 293 cells (HEK293). It contains AA Ser 22 - Arg 200 (Accession # Q8TDQ0-1).

 

Molecule : TIM-3

 

Synonyms : HAVCR2,TIM3,TIMD3,FLJ14428,KIM3

 

Format : Powder

 

Category : MABSol® Biotin Labeled Proteins

 

Accession : NP_116171.3

 

Storage : -20℃

 

Shipping condition : Powder,RT

 

Molecular Weight : 23.1 kDa

 

Characteristics :

This protein carries an Avi tag (Avitag™) at the C-terminus, followed by a polyhistidine tag. The protein has a calculated MW of 23.1 kDa. The protein migrates as 40-50 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.

 

Buffer : PBS, pH7.4

 

Description :

Hepatitis A virus cellular receptor 2 is also known as HAVCR2, FLJ14428, KIM3, TIM3, TIMD3, is a member of the TIM family of immune regulating molecules with one Ig-like V-type domain and a Ser/Thr-rich mucin stalk. CD4-positive T helper lymphocytes can be divided into types 1 (Th1) and 2 (Th2) on the basis of their cytokine secretion patterns. Th1 cells and their associated cytokines are involved in cell-mediated immunity to intracellular pathogens and delayed-type hypersensitivity reactions, whereas Th2 cells are involved in the control of extracellular helminthic infections and the promotion of atopic and allergic diseases. The 2 types of cells also cross-regulate the functions of the other. HAVCR2 is a Th1-specific cell surface protein that regulates macrophage activation and enhances the severity of experimental autoimmune encephalomyelitis in mice. HAVCR2 regulates macrophage activation. Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance. May be also involved in T-cell homing. Dysregulation of the HAVCR2-galectin-9 pathway could underlie chronic autoimmune disease states in human, such as multiple sclerosis.

 

References :

(1)Monney, L. et al., 2002, Nature, 415:536-541.
(2)Sabatos, CA. et al., 2003, Nat. Immunol., 4:1102-1110.
(3)Anderson, AC. et al., 2006, Curr. Opin. Immunol., 18:665-669.