普健生物（武汉）科技有限公司（AtaGenix）
Recombinant Human CD40 protein ,C- His Tag
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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 CD40 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 CD40(Met1~Arg193) was fused with the C-terminal His Tag
Accession #
P25942
表达宿主（Host）
Mammalian cells
种属（Species）
Homo sapiens (Human)
预测分子量（Predicted Molecular Mass）
22.32kDa
制剂（Formulation）
Supplied as solution form in PBS, pH7.5 or lyophilized from PBS, pH7.5.
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.
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
Tumor necrosis factor receptor superfamily member 5 (TNFRSF5) is also known as CD40, is a member of the TNF receptor superfamily. The expression of CD40 is diverse. TNFRSF5 has been found to be essential in mediating a broad variety of immune and inflammatory responses including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation. CD40 is the receptor for TNFSF5/CD40LG. Defects in CD40 are the cause of immunodeficiency with hyper-IgM type 3 (HIGM3).
分子别名（Alternative Names）
CD40,Bp50,CDW40,MGC9013,TNFRSF5,p50
参考文献（References）
Marzaioli, Canavan, Floudas, Wade, Low, Veale, Fearon (2020) Monocyte-Derived Dendritic Cell Differentiation in Inflammatory Arthritis Is Regulated by the JAK/STAT Axis via NADPH Oxidase Regulation Frontiers in immunology 11() 1406
Noteicon
For research use only .
Monocyte-derived Dendritic cells (Mo-DC) are a distinct DC subset, involved in inflammation and infection, they originate from monocytes upon stimulation in the circulation and their activation and function may vary in autoimmune diseases. In this study we investigate the differences in Mo-DC differentiation and function in patients with Rheumatoid (RA) compared to Psoriatic arthritis (PsA). A significant increase in the Mo-DC differentiation marker CD209, paralleled by a corresponding decrease in the monocytic marker CD14, was demonstrated in RA compared to PsA, as early as 1 day post Mo-DC differentiation. RA monocytes ex-vivo were phenotypically different to PsA, displaying a more mature phenotype associated with altered cellular-morphology, early dendrite formation, and a significant increase in the CD40 marker. In addition, SPICE algorithm flow cytometric analysis showed distinct differences in chemokine receptors distribution in HC compared to PsA and RA CD14+ cells in the blood, with increased expression of the chemokine receptors CCR7 and CXCR4 observed in PsA and RA. In addition CD14+ cells at the site of inflammation showed a different chemokine receptor pattern between PsA and RA patients, with higher expression of CXCR3 and CXCR5 in RA when compared to PsA. The early priming observed in RA resulted in monocyte-endocytosis and antigen-uptake mechanisms to be impaired, effects that were not observed in PsA where phagocytosis capacity remained highly functional. Tofacitinib inhibited early Mo-DC differentiation, decreasing both CD209 and CD40 activation markers in RA. Inhibition of Mo-DC differentiation in response to Tofacitinib was mediated via an imbalance in the activation of NADPH-oxidases NOX5 and NOX2. This effect was reversed by NOX5 inhibition, but not NOX2, resulting in suppression of NOX5-dependent ROS production. In conclusion, RA monocytes are already primed ex vivo to become DC, evident by increased expression of activation markers, morphological appearance and impaired endocytosis capacity. Furthermore, we demonstrated for the first time that NOX5 mediates Mo-DC differentiation and function in response to Tofacitinib, which may alter DC functions.
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