Mouse TIM-3 / HAVCR2 Protein, His Tag
Proteins and Peptides
- 貨號 Cat. No.
- TI3-M52H1
- 規格 Size
- 100ug
- 品牌 Brand
- ACROBiosystems
- Species
- Mouse
- Conjugate
- Unconjugated
- Expression System
- HEK293
- Tag
- His Tag
Description
Source :
Mouse TIM-3, His Tag (TI3-M52H1) is expressed from human 293 cells (HEK293). It contains AA Arg 20 - Arg 191 (Accession # AAL65156.1).
Molecule : TIM-3
Synonyms : HAVCR2,TIM3,TIMD3,FLJ14428,KIM3
Format : Powder
Category : Immune Checkpoint Proteins
Accession : N/A
Storage : -20℃
Shipping condition : Powder,RT
Molecular Weight : 21.0 kDa
Characteristics :
This protein carries a polyhistidine tag at the C-terminus. The protein has a calculated MW of 21.0 kDa. The protein migrates as 33-47 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: 536-41.
(2) Sabatos, CA. et al., 2003, Nat. Immunol. 4: 1102-10.
(3) Anderson, AC. et al., 2006, Curr. Opin. Immunol. 18: 665-9.

