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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N1609 Ginsenoside Rh2 -
N1610 Ginsenoside Rh1 -
N1613 Ginsenoside Rg11 CitationTarget: Glucocorticoid ReceptorsSummary: Triterpene saponins/steroid glycosides found in Panax -
N1620 Ginsenoside Rb1Summary: Antiproliferative agent -
N1622 Panaxadiol -
N1625 FormononetinSummary: O-methylated isoflavone -
N1633 Eleutheroside E -
N1638 Peiminine -
N1647 Tectorigenin -
A1094 tumor protein p53 binding protein fragment [Homo sapiens]/[Mus musculus]Summary: P53 binding protein fragment


