Galectin-9 (Gal-9) is a member of animal lectins that have an affinity to β-galactosides and Forssman pentasaccharide. It is strongly overexpressed in Hodgkin′s disease tissue and it might participate in the interaction between the H&RS cells with their surrounding cells and might thus play a role in the pathogenesis of this disease and/or its consistently associated immunodeficiency. Recombinant Galectin-9 protein was expressed in E.coli and purified by using conventional chromatography techniques.
Physikalische Form
0.5 mg/mL in 20 mM Tris-HCl buffer (pH 8.0) containing 1 mM NaCl and 20% glycerol.
Lagerklassenschlüssel
13 - Non Combustible Solids
WGK
WGK 3
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
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The Journal of pathology, 245(4), 468-477 (2018-05-08)
In patients with metastatic melanoma, high blood levels of galectin-9 are correlated with worse overall survival and a bias towards a Th2 inflammatory state supportive of tumor growth. Although galectin-9 signaling through TIM3 on T cells has been described, less
Patients with autoimmune thyroid disease (AITD) show defects in their immune-regulatory mechanisms. Herein we assessed the expression and function of galectin-1 and galectin-9 (Gal-1, Gal-9) in dendritic cells (DCs) from patients with AITD. Peripheral blood samples from 25 patients with
T cell immunoglobulin and mucin protein 3 (TIM-3) is a type I cell surface protein that was originally identified as a marker for murine T helper type 1 cells. TIM-3 was found to negatively regulate murine T cell responses and
Journal of dermatological science, 96(3), 134-142 (2019-12-04)
Galectin-9, a member of the galectin family, can promote tumor growth through inducing apoptosis in anti-tumor immune cells via T cell immunoglobulin and mucin domain 3 (TIM-3). On the other hand, galectin-9 also induces tumor cell apoptosis in many malignancies
The S-type lectin galectin-9 binds to the negative regulatory molecule Tim-3 on T cells and induces their apoptotic deletion or functional inactivation. We investigated whether galectin-9/Tim-3 interactions contribute to the deletion and exhaustion of the antiviral T cell response in
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