普健生物(武汉)科技有限公司(AtaGenix)

Recombinant Human TNFRSF18 protein ,C- His Tag

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ATMP00491HU
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  • 产品信息(Product Details)
  • 前沿进展(Frontier progress)
  • 如何订购
  • 说明书
概述(Summary)icon
英文全称
Recombinant Human TNFRSF18 protein ,C- His Tag
纯度(Purity)
>90% as determined by SDS-PAGE
内毒素(Endotoxin level)
Please contact with the lab for this information.
蛋白构建(Construction)
A DNA sequence encoding the human TNFRSF18(Met1-Glu161) was fused with the C-terminal His Tag
Accession #
Q9Y5U5
表达宿主(Host)
Mammalian cells
种属(Species)
Homo sapiens (Human)
预测分子量(Predicted Molecular Mass)
17.71kDa
制剂(Formulation)
Supplied as solution form in PBS or lyophilized from PBS .
运输方式(Shipping)
In general, proteins are provided as lyophilized powder/frozen liquid. They are shipped out with dry ice/blue ice unless customers require otherwise.
稳定性&储存(Stability &Storage)
Use a manual defrost freezer and avoid repeated freeze thaw cycles.
Store at 2 to 8 °C for one week .
Store at -20 to -80 °C for twelve months from the date of receipt.
复溶(Reconstitution)
Reconstitute in sterile water for a stock solution.A copy of datasheet will be provided with the products, please refer to it for details.
电泳图(SDS-PAGE image)icon
    背景(Background)icon
    背景介绍
    Glucocorticoid-induced TNFR-related protein (GITR) is also known as Tumor necrosis factor receptor superfamily member 18 (TNFRSF18), activation-inducible TNFR family receptor (AITR), CD antigen CD357, which is a member of the tumor necrosis factor receptor (TNF-R) superfamily. GITR is receptor for TNFSF18, which seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. GITR also mediated NF-kappa-B activation via the TRAF2/NIK pathway.
    分子别名(Alternative Names)
    AITR,GITR,TNFRSF18,CD357
    参考文献(References)
    Puntigam, Jeske, Götz, Greiner, Laban, Theodoraki, Doescher, Weissinger, Brunner, Hoffmann, Schuler (2020) Immune Checkpoint Expression on Immune Cells of HNSCC Patients and Modulation by Chemo- and Immunotherapy International journal of molecular sciences 21(15)
    Noteicon
    For research use only .
    Endogenous control mechanisms, including immune checkpoints and immunosuppressive cells, are exploited in the process of tumorigenesis to weaken the anti-tumor immune response. Cancer treatment by chemotherapy or immune checkpoint inhibition can lead to changes of checkpoint expression, which influences therapy success. Peripheral blood lymphocytes (PBL) and tumor-infiltrating lymphocytes (TIL) were isolated from head and neck squamous cell carcinoma (HNSCC) patients (n = 23) and compared to healthy donors (n = 23). Immune checkpoint expression (programmed cell death ligand 1 (PD-1), tumor necrosis factor receptor (TNFR)-related (GITR), CD137, tumor necrosis factor receptor superfamily member 4 (TNFRSF4) (OX40), t-cell immunoglobulin and mucin-domain containing-3 (TIM3), B- and T-lymphocyte attenuator (BTLA), lymphocyte-activation gene 3 (LAG3)) was determined on immune cells by flow cytometry. PD-L1 expression was detected on tumor tissue by immunohistochemistry. Immune cells were treated with immuno- and chemotherapeutics to investigate treatment-specific change in immune checkpoint expression, in vitro. Specific changes of immune checkpoint expression were identified on PBL and TIL of HNSCC patients compared to healthy donors. Various chemotherapeutics acted differently on the expression of immune checkpoints. Changes of checkpoint expression were significantly less pronounced on regulatory T cells compared to other lymphocyte populations. Nivolumab treatment significantly reduced the receptor PD-1 on all analyzed T cell populations, in vitro. The specific immune checkpoint expression patterns in HNSCC patients and the investigated effects of immunomodulatory agents may improve the development and efficacy of targeted immunotherapy.

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