Cell membrane blebbing, chromatin condensation, genomic DNA fragmentation, and the exposure of particular phagocytosis signaling molecules on the cell surface are just a few of the distinctive morphological and biochemical features of the cell death process known as apoptosis. Apoptosis-initiated cell death is distinct from necrosis-induced cell death. Apoptotic death, in contrast, is silent and orderly. Necrotic cells are typically recognized as a danger signal by the immune system, which causes inflammation.

There are two main methods for inducing apoptotic cell death: The intrinsic pathway, also known as the Bcl-2-regulated or mitochondrial pathway, is strictly regulated by the BCL-2 family of proteins and is activated by a variety of developmental cues or cytotoxic insults, such as viral infection, DNA damage, and growth-factor deprivation.The tumor necrosis factor (TNF) receptor family members, such as Fas or TNF receptor-1 (TNFR1), which contain an intracellular death domain and can recruit and activate caspase-8 through the adaptor protein Fas-associated death domain (FADD; also known as MORT1) at the cell surface, are what initiate the extrinsic or death-receptor pathway. Without the involvement of the BCL-2 family, this recruitment results in the subsequent activation of downstream (effector) caspases like caspase-3, -6, or -7.

Numerous human diseases, including cancer, viral infections, autoimmune diseases, neurodegenerative disorders, and AIDS (acquired immunodeficiency syndrome), may be influenced by changes in cell survival, according to studies. Some of these diseases may not progress naturally unless specific therapies that change the apoptotic threshold are used.

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