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BD Pharmingen- FITC Active Caspase-3 Apoptosis Kit_BD Pharmingen

产品信息
抗原名称
Caspase-3
简单描述
The caspase family of cysteine proteases plays a key role in apoptosis and inflammation. Caspase-3 is a key protease that is activated during the early stages of apoptosis and, like other members of the caspase family, is synthesized as an inactive pro-enzyme that is processed in cells undergoing apoptosis by self-proteolysis and/or cleavage by another protease. The processed forms of caspases consist of large (17-22 kDa) and small (10-12 kDa) subunits which associate to form an active enzyme. Active caspase-3, a marker for cells undergoing apoptosis, consists of a heterodimer of 17 and 12 kDa subunits which is derived from the 32 kDa pro-enzyme. Active caspase-3 proteolytically cleaves and activates other caspases, as well as relevant targets in the cytoplasm, e.g., D4-GDI and Bcl-2, and in the nucleus (e.g. PARP).  This antibody has been reported to specifically recognize the active form of caspase-3 in human and mouse cells.  It has not been reported to recognize the pro-enzyme form of caspase-3.
克隆号
(RUO)
BD化合物表
  • 描述
    数量/尺寸
    零件号
    EntrezGene ID
  • FITC Rabbit Anti- Active Caspase-3
    100 Tests (1 ea)
    51-68654X
    N/A
  • Cytofix/Cytoperm™ Fixation and Permeabilization Solution (1X)
    N/A
    51-6896KC
    N/A
  • Perm/Wash™ Buffer (10X Solution)
    N/A
    51-6897KC
    N/A
应用
实验应用
Intracellular staining (flow cytometry) (Routinely Tested)
反应种属
Human (QC Testing), Mouse (Tested in Development)
目标/特异性
Active Caspase-3 (Cpp32)
文献
文献
研发参考(3) 1. Alnemri ES, Livingston DJ, Nicholson DW, et al. Human ICE/CED-3 protease nomenclature. Cell. 1996; 87(2):171. (Biology). 2. Fujita N, Tsuruo T. Involvement of Bcl-2 cleavage in the acceleration of VP-16-induced U937 cell apoptosis. Biochem Biophys Res Commun. 1998; 246(2):484-488. (Biology). 3. Patel T, Gores GJ, Kaufmann SH. The role of proteases during apoptosis. FASEB J. 1996; 10(5):587-597. (Biology).

参考图片

Flow cytometric analysis of apoptotic and non-apoptotic populations for active caspase-3. Jurkat cells (Human T-cell leukemia; ATCC TIB-152) were left untreated (left panel) or treated for 4 hr with camptothecin (right panel) to induce apoptosis. Cells were permeabilized, fixed, and stained for active caspase-3 as described in the accompanying Staining Protocol. Cells were then analyzed by flow cytometry. Untreated cells were primarily negative for the presence of active caspase-3, whereas greater than one third of the treated cells were positive for active caspase-3 staining (right panel, M2).

Flow cytometric analysis of apoptotic and non-apoptotic populations for active caspase-3. Jurkat cells (Human T-cell leukemia; ATCC TIB-152) were left untreated (left panel) or treated for 4 hr with camptothecin (right panel) to induce apoptosis. Cells were permeabilized, fixed, and stained for active caspase-3 as described in the accompanying Staining Protocol. Cells were then analyzed by flow cytometry. Untreated cells were primarily negative for the presence of active caspase-3, whereas greater than one third of the treated cells were positive for active caspase-3 staining (right panel, M2).

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