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      FITC標記 Anti-Bcl2 (流式Flow Cyt)單克隆抗體abcam(ab93502)

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      • 公司名稱上海博耀生物科技有限公司
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      • 更新時間2016/3/15 12:08:13
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      Anti-Bcl2

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      Anti-Bcl2 antibody [10C4] (FITC) (ab93502)
      DescriptionMouse monoclonal [10C4] to Bcl2 (FITC)
      FITC標記 Anti-Bcl2 (流式Flow Cyt)單克隆抗體abcam(ab93502) 產品信息

      FunctionSuppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).

      • Tissue specificityExpressed in a variety of tissues.
      • Involvement in diseaseNote=A chromosomal aberration involving BCL2 has been found in chronic lymphatic leukemia. Translocation t(14;18)(q32;q21) with immunoglobulin gene regions. BCL2 mutations found in non-Hodgkin lymphomas carrying the chromosomal translocation could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions.
      • Sequence similaritiesBelongs to the Bcl-2 family.
      • DomainThe BH4 motif is required for anti-apoptotic activity and for interaction with RAF1 and EGLN3.
      • Post-translational
        modifications
        Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity. Growth factor-stimulated phosphorylation on Ser-70 by PKC is required for the anti-apoptosis activity and occurs during the G2/M phase of the cell cycle. In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases. Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-87, wich stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A).
        Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity, causes the release of cytochrome c into the cytosol promoting further caspase activity.
        Monoubiquitinated by PARK2, leading to increase its stability.
      • Cellular localizationMitochondrion outer membrane. Nucleus membrane. Endoplasmic reticulum membrane.
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