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Phospho-TNFR(S274) Antibody

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  • $495
  • Leading Biology
  • APR05157G
  • 2026年03月31日
  • WB, IHC-P, E
  • Rabbit
  • Human, Mouse
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 亚型

      Rabbit Ig

    • 保存条件

      Store at +4°C short term. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.

    • 适应物种

      Human, Mouse

    • 库存

      100

    • 宿主

      Rabbit

    • 应用范围

      WB, IHC-P, E

    • 靶点

      This TNFR Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S274 of human TNFR.

    • 规格

      100 μl

    Prouduct: We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality Phospho-TNFR(S274) Antibody. Functiong: Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate- specific cysteine proteases) mediating apoptosis. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. Summary: A member of the TNF-receptor superfamily, this protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the autosomal dominant periodic fever syndrome. The impaired receptor clearance is thought to be a mechanism of the disease.

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