Apoptosis, also known as programmed cell death, is rigorously controlled process of cell death that leads to phagocytosis of unwanted cell. It is triggered after sufficient cellular damage and activated through extrinsic or intrinsic pathways. The intrinsic pathway is mainly occurs via release of cytochrome c from the mitochondria and regulates mitochondrial outer membrane permeabilization by Bcl-2 family proteins. The extrinsic pathway is induced by ligand binding to death receptor, such as Fas, TNFαR, DR3, DR4, and DR5. Caspases then cleave target proteins and nuclear lamins to promote DNA degradation, resulting apoptotic cells undergo phagocytosis. In addition, p53 has the ability to activate intrinsic and extrinsic pathways of apoptosis by inducing transcription of several proteins like Puma, Bid, Bax, TRAIL-R2, and CD95.
Some Inhibitors of apoptosis proteins (IAPs), such as XIAP/BIRC4 and Bruce/BIRC6, can block casapse activity through direct binding, while other IAPs, such as cIAP1/BIRC2, cIAP2/BIRC3, act as ubiquitin ligases that target caspases for ubiquitin-mediated degradation. Apoptosis is essential for growth, development and aging in multicellular organisms. Any alterations or abnormalities occurring in apoptotic processes contribute to development of human diseases, including cancer.
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- A8783 VU661013Summary: Novel, potent, selective MCL-1 inhibitor
- B6023 PD-1/PD-L1 inhibitor 2Target: PD-1/PD-L1 interactionSummary: PD-1/PD-L1 interaction inhibitor
- C7117 D-Pantothenate sodium
- C7092 Triglycidyl Isocyanurate (Teroxirone)
- C6983 Citicoline
- C6964 Diatrizoic acid
- C6880 Vanillyl alcohol
- C6591 Taurochenodeoxycholic acid sodium salt
- C6526 Diatrizoate sodium
- A1902 Z-VAD-FMK102 CitationTarget: CaspasesSummary: Cell-permeable, irreversible pan-caspase inhibitor