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Galectin-9 (human):Fc (human) (rec.)

CHI-HF-210GAL9-C050 50 µg INQ
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Additional Information

Product Data
Synonyms Gal-9; Ecalectin; TIM3L; TIM-3 Ligand; T Cell Immunoglobulin and Mucin Domain-containing Protein 3 Ligand
Properties
Source/Host HEK 293 cells
Sequence The extracellular domain of human Galectin-9 (aa 2-323) is fused to the N-terminus of the Fc region of human IgG1.
Crossreactivity Human
Biological Activity Measured by its binding ability in a functional ELISA.
MW ~70kDa (SDS-PAGE)
Purity ≥95% (SDS-PAGE)
Endotoxin Content <5EU/mg protein (LAL test; Lonza).
Reconstitution Reconstitute with 50 µl sterile water. Add 1X PBS to the desired protein concentration.
Formulation Lyophilized from 0.2μm-filtered solution in PBS.
Other Product Data NCBI reference AAI05943.1: Galectin-9 (human)
Origin Manufactured by Chimerigen.
Product Type Protein
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Handling Advice Avoid freeze/thaw cycles.
Use/Stability Stable for at least 1 year after receipt when stored at -20°C. Working aliquots are stable for up to 3 months when stored at -20°C.
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Product Description

The TIM (T cell/transmembrane, immunoglobulin and mucin) family plays a critical role in regulating immune responses, including allergy, asthma, transplant tolerance, autoimmunity and the response to viral infections. The unique structure of TIM immunoglobulin variable region domains allows highly specific recognition of phosphatidylserine (PtdSer), exposed on the surface of apoptotic cells. Tim-3, a type I transmembrane protein, contains an immunoglobulin and a mucin-like domain in its extracellular portion and a tyrosine phosphorylation motif in its cytoplasmic portion. TIM-3 is preferentially expressed on Th1 and Tc1 cells, and generates an inhibitory signal resulting in apoptosis of Th1 and Tc1 cells. TIM-3 is also expressed on some dendritic cells and can mediate phagocytosis of apoptotic cells and cross-presentation of antigen. Tim-3 functions to inhibit aggressive Th1-mediated auto- and alloimmune responses. Tim-3 pathway blockade by administration of Tim-3:Fc fusion protein accelerates diabetes in nonobese diabetic mice, causes hyperproliferation of Th1 cells and Th1 cytokine release in an experimental autoimmune encephalomyelitis (EAE) model and prevents acquisition of transplantation tolerance induced by costimulation blockade.
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