CD40 / TNFRSF5 / Bp50抗体

CD40 / TNFRSF5 / Bp50抗体

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  • 询价
  • Abcam
  • 中国/美国/德国
  • xy10774-RP01
  • 2025年07月12日
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    • 保存条件

      常温,避光

    • 克隆性

      单克隆

    • 抗体名

      CD40 / TNFRSF5 / Bp50抗体

    CD40 / TNFRSF5 / Bp50抗体产品信息免疫原 : Recombinant human CD40 protein ( Catalog#10774-H08H )

    Antibody Type : Rabbit Polyclonal Antibody ( Antibody Purification Platform )
    抗体宿主 : Rabbit IgG

    缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
    制备方法 : Produced in rabbits immunized with purified, human cell-derived, recombinant human CD40 extracellular domain ( rh CD40; Catalog#10774-H08H; NP_001241.1; Met 1 - Arg 193 ). Total IgG was purified by Protein A affinity chromatography
    CD40 / TNFRSF5 / Bp50抗体背景综述

    Human tumor necrosis factor receptor superfamily member 5, also known as CD40 and TNFRSF5, is a member of the TNF receptor superfamily which are single transmembrane-spanning glycoproteins, and plays an essential role 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 contains 4 cysteine-rich repeats in the extracellular domain, and is expressed in B cells, dendritic cells, macrophages, endothelial cells, and several tumor cell lines. The cognate interaction between CD40 and CD40 ligand (CD154) on T cells activates NF-kappa B, Jun N-terminal kinase, and Janus kinase signal transducers and activators of transcription pathways. Several different TRAF proteins (Adaptor proteins) have been identified to serves as mediators of the signal transduction. In addition, CD40/CD40L interaction is found to be necessary for amyloid-beta-induced microglial activation, and thus is thought to be an early event in Alzheimer disease pathogenesis. Defects in CD40 result in hyper-IgM immunodeficiency type 3 (HIGM3), an autosomal recessive disorder characterized by an inability of B cells to undergo isotype switching, as well as an inability to mount an antibody-specific immune response, and a lack of germinal center formation.
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