Apoptosis
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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B4653 BV629 CitationSummary: Selective inhibitor of IAP proteins -
B4677 NVP-CGM097Summary: potent and selective MDM2 inhibitor -
B7535 Eeyarestatin ITarget: ERADSummary: inhibitor of endoplasmic reticulum-associated degradation (ERAD) and protein translocation -
B5734 3-Nitropropionic acidSummary: Mitochondrial respiratory complex II (succinate dehydrogenase) inhibitor -
C6591 Taurochenodeoxycholic acid sodium salt -
C6880 Vanillyl alcohol -
C6921 Phenanthrene -
C6964 Diatrizoic acid -
C6983 Citicoline -
C7092 Triglycidyl Isocyanurate (Teroxirone)


