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Mouse Anti-Human CD95 Antibody (DX2)

Tumor necrosis factor receptor superfamily member 6,Apo-1 antigen,Apoptosis-mediating surface antigen FAS,FASLG receptor,APT1,FAS1,TNFRSF6,FAS

价格 600.00 1-2周
货号 S0B5637
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产品规格
  • 宿主来源

    Mouse
  • 抗原名称

    CD95
  • 分子别名

    Tumor necrosis factor receptor superfamily member 6; Apo-1 antigen; Apoptosis-mediating surface antigen FAS; FASLG receptor; APT1; FAS1; TNFRSF6; FAS
  • 细胞定位

    Cell membrane
  • Accession

    P25445
  • 克隆号

    DX2
  • 抗体类型

    Mouse mAb
  • 抗体同种型

    IgG1,k
  • 反应种属 ?

    RhMk, CyMk, Hu
  • 阳性样本

    Human Peripheral Blood cells
  • 纯化方式

    Protein G
  • 浓度

    2 mg/ml
  • 标记

    Unconjugated
  • 性状

    Liquid
  • 缓冲体系

    PBS pH7.4

  • 储存条件

    12 months from date of receipt / reconstitution, 2 to 8 °C as supplied

  • 应用

    FCM

  • 稀释度

    应用 稀释度 推荐种属
    FCM 1:200 Hu
背景介绍
  • CD95, also known as Fas or APO-1, is a protein that plays a crucial role in the regulation of apoptosis, or programmed cell death. It is a member of the tumor necrosis factor receptor superfamily and is expressed on the surface of various immune cells, including T cells and B cells. When CD95 is engaged by its ligand, CD95L, it triggers a signaling cascade involving the recruitment of adaptor proteins such as FADD, which in turn activates caspases, leading to the dismantling of the cell. This pathway is essential for maintaining immune homeostasis by eliminating activated or damaged cells. Dysregulation of CD95 signaling has been implicated in a range of diseases, including autoimmune disorders and cancer, highlighting its importance in both physiological and pathological contexts.

  • 流式分析

    • Flow cytometric analysis of Human Peripheral Blood cells labelling Human CD95 antibody at 1/200 dilution (1 μg) / (Red) compared with Mouse IgG1, κ Isotype Control (Black) isotype control and an unlabelled control (cells without incubation with primary antibody and secondary antibody) (Blue). Goat Anti - Mouse IgG Alexa Fluor® 488 was used as the secondary antibody.

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