Name: Mouse TIM-3/HAVCR2 Recombinant Protein (Fc Tag)

Synonyms: Hepatitis A virus cellular receptor 2 homolog;HAVcr-2;T-cell immunoglobulin and mucin domain-containing protein 3;T-cell immunoglobulin mucin receptor 3;T-cell membrane protein 3;Tim3;Timd3

Expression host: HEK293 Cells

Sequence: Arg20-Arg191

Accesstion: Q8VIM0

Species: Mouse

Mol_Mass: 46.3 kDa

AP_Mol_Mass: 50-80 kDa

Tag: C-Fc

Purity: > 95 % as determined by reducing SDS-PAGE.

Endotoxin:

Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Formulation: Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.Please refer to the specific buffer information in the printed manual.

Reconstitution: Please refer to the printed manual for detailed information.

Background: T cell immunoglobulin and mucin domain-3 (TIM3), also called hepatitis A virus cellular receptor 2 (HAVCR2), is a transmembrane glycoprotein of the TIM family of immune regulating molecules and plays an important role in the Th1-mediated immune response. TIM3 is expressed on the Th1 cells, CD8 T-cells, monocytes, and dendritic cells, but not on Th2 cells. TIM3 expressed by monocytes and dendritic cells facilitates phagocytosis of apoptotic cells and up-regulates cross-presentation of apoptotic cell-associated antigens through interaction with phosphatidylserine. Engagement of TIM3 by its ligand galectin-9 induces a range of immunosuppressive functions which enhance immune tolerance and inhibit anti-tumor immunity. Stimulation of TIM3 with an agonistic antibody promotes inflammation through the activation of innate immune cells. TIM3 is also regarded as a potential target molecule for immunotherapy. TIM3 and programmed cell death 1 (PD-1) as two important coinhibitory regulators of T cell responses, have been implicated with the T-cell dysfunction or exhaustion associated with chronic HBV infection including HBV-related HCC.

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