Alexa Fluor® 647 Anti-Protein CASP antibody [EPR18806]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Protein CASP also known as Caspase or CASP protein is an important player in the process of apoptosis. Caspases are cysteine-aspartic proteases that exist as inactive proenzymes made of a prodomain large and small subunits. Upon activation caspases cleave substrates after aspartic acid residues. The Caspase family proteins have similar structures with molecular masses around 20 kDa to 40 kDa. CASP proteins are widely expressed across different tissues in the body. Activation can happen through intrinsic and extrinsic pathways enabling them to mediate the orderly dismantling of cellular components.

Biological function summary

Protein CASP acts as an executioner enzyme in cell death. It forms part of intricate protein complexes notably the apoptosome which includes APAF1 and cytochrome c. Once activated CASP proteins initiate a cascade of proteolytic events that lead to the dismantling of the cell. This process is tightly regulated and is essential for maintaining homeostasis and tissue development. Other caspases work upstream to activate downstream executioner caspases further highlighting the protein's role in these biological functions.

Pathways

Protein CASP plays a significant role in apoptotic signaling pathways. It is pivotal in both the extrinsic and intrinsic apoptotic pathways. In the extrinsic pathway proteins such as FADD and DISC interact with CASP-8 to trigger apoptosis. The intrinsic pathway includes the release of cytochrome c which partners with APAF1 leading to the activation of CASP-9 and subsequently other caspases. This cascade illustrates the interconnected nature of apoptotic signaling with other molecular pathways ensuring the precise regulation of cell death.

Associated diseases and disorders

Protein CASP is associated with cancer and neurodegenerative diseases. Dysregulation of CASP activity can result in either excessive cell death or survival contributing to disease pathogenesis. In cancers often CASP activity is impaired allowing cancer cells to evade apoptosis and proliferate unchecked. In neurodegenerative disorders such as Alzheimer's abnormal CASP activation contributes to neuronal loss. The interaction between CASP proteins and BCL-2 family members highlights their role in these diseases emphasizing the therapeutic targeting potential in modulating CASP activity.