Phospho-p53 (Ser15) cellular kit
Assay kit for the detection of Phospho-p53 (Ser15)
The cleaved PARP (Asp214) kit enables the specific and quantitative detection of endogenous levels of the human, mouse, and monkey large fragment (89-kDa) of PARP-1. With its central position downstream from caspases 3 and 7, both activated by extrinsic and intrinsic apoptosis pathways, cleaved PARP-1 represents a pertinent marker of cells undergoing apoptosis. Deregulated apoptosis plays a role in various diseases involving insufficient cell death, such as cancer, autoimmunity, and persistent infections, whereas excessive apoptosis can contribute to neuro-degeneration and ischaemia.
Two pathways activate the effector pro-caspase 3 that cleaved PARP on Asp214, leading to apoptosis:
- an extrinsic pathway (activated by death ligands like TNF alpha, FasL and ApoL that bind to their death receptors), activating the initiator procaspase-8
- an intrinsic pathway, or mitochondrial pathway (activated by cellular damage like stress, radiation, toxins, hypoxia and growth factor withdrawal), also activating pro-apoptotic factors like BAD, then the initiator procaspase-9
In response to death ligands or cell damage and activation of extrinsic or intrinsic apoptosis pathways, the nuclear enzyme PARP-1 (116 kDa) involved in the repair of damaged DNA is cleaved between Asp214 and Gly215 by activated caspases 3 and 7. The cleavage deactivates the enzyme by separating its N-terminal DNA binding domain p25 (24kDa) from its C-terminal catalytic domain p85 (89kDa), leading to DNA fragmentation and cell apoptosis. Cleaved PARP-1 is considered as an essential marker of apoptosis.
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