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Mouse TIM3 / HAVCR2 Protein (Fc Tag)

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Mouse TIM3 Protein Product Information
Synonym:HAVCR2, Tim3, Timd3
Protein Construction:A DNA sequence encoding the mouse HAVCR2 (AAL65156.1) (Met1-Arg191) was expressed with the Fc region of human IgG1 at the C-terminus.
Expressed Host:Human Cells
Shipping:In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.
Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Mouse TIM3 Protein QC Testing
Purity:> 95 % as determined by SDS-PAGE
Endotoxin:< 1.0 EU per μg of the protein as determined by the LAL method
Stability:Samples are stable for up to twelve months from date of receipt at -70℃
Predicted N Terminal:Leu 22
Molecule Mass:The recombinant mouse HAVCR2/Fc is a disulfide-linked homodimer. The reduced monomer comprises 411 amino acids and has a predicted molecular mass of 45.9 kDa. The apparent molecular mass of the protein is approximately 58-66 kDa in SDS-PAGE under reducing conditions due to glycosylation.
Formulation:Lyophilized from sterile PBS, pH 7.4.
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
Mouse TIM3 Protein Usage Guide
Storage:Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Reconstitution:A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Mouse TIM3 Protein SDS-PAGE
Mouse TIM3 / HAVCR2 Protein (Fc Tag) SDS-PAGE
Other TIM3 Recombinant Protein Products
TIM-3/HAVCR2  Background

Hepatitis A virus cellular receptor 2 (HAVCR2), formerly known as T cell immunoglobulin and mucin domain-3 (TIM-3), is a transmembrane glycoprotein expressed on the surface of terminally differentiated Th1 cells but not on Th2 cells. It was the first surface molecule that specifically identifies Th1 cells in both mice and human. Recently, identification of Galectin-9 as a ligand for TIM-3 has established the TIM-3-Galectin-9 pathway as an important regulator of Th1 immunity and tolerance induction. Engagement of Tim-3 by its ligand galectin-9 negatively regulates IFN-gamma secretion and influences the ability to induce T cell tolerance in both mice and man. It suggests a novel paradigm in which dysregulation of the TIM-3-galectin-9 pathway could underlie chronic autoimmune disease states, such as multiple sclerosis. Recent work has explored the role of TIM-3 in systemic lupus erythematosus (SLE), and their results indicate that TIM-3 may represent a novel target for the treatment of SLE. Numerous studies have demonstrated that Tim-3 influences autoimmune diseases, including diabetes and multiple sclerosis, and its role in other inflammatory diseases including allergies and cancer is beginning to become clear. In tumor rejection model, soluble form of Tim-3 (sTim-3) significantly impaired T cell antitumor immunity, evidenced by decreased antitumor CTL activity and reduced amount of tumor-infiltrating lymphocytes in tumor. sTim-3 as an immunoregulatory molecule that may be involved in the negative regulation of T cell-mediated immune response.

Mouse TIM-3/HAVCR2  References
  • Geng H, et al. (2006) Soluble form of T cell Ig mucin 3 is an inhibitory molecule in T cell-mediated immune response. J Immunol. 176(3): 1411-20.
  • Anderson AC, et al. (2006) TIM-3 in autoimmunity. Curr Opin Immunol. 18(6): 665-9.
  • Anderson DE. (2007) TIM-3 as a therapeutic target in human inflammatory diseases. Expert Opin Ther Targets. 11(8): 1005-9.
  • Pan HF, et al. (2010) TIM-3 as a new therapeutic target in systemic lupus erythematosus. Mol Biol Rep. 37(1): 395-8.
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    Catalog: 51152-M02H-50
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    All information of our products is subject to change without notice. Please refer to COA enclosed in shipped package for the newest information.