Apoptosis by death factor.
TLDR
This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.About:
This article is published in Cell.The article was published on 1997-02-07 and is currently open access. It has received 5054 citations till now.read more
Citations
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Journal ArticleDOI
Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
Anne Brunet,Azad Bonni,Michael J. Zigmond,Michael Z. Lin,Peter Juo,Linda Hu,Michael J. Anderson,Karen C. Arden,John Blenis,Michael E. Greenberg +9 more
TL;DR: It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
Journal ArticleDOI
Cellular survival: a play in three Akts
TL;DR: The mechanisms by which survival factors regulate the PI3K/c-Akt cascade, the evidence that activation of the PI 3K/ c-AKT pathway promotes cell survival, and the current spectrum of c- akt targets and their roles in mediating c- Akt-dependent cell survival are reviewed.
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Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors
TL;DR: The purification of a cytosolic protein that induces cytochrome c release from mitochondria in response to caspase-8, the apical caspases activated by cell surface death receptors such as Fas and TNF is reported.
Journal ArticleDOI
BCL-2 family members and the mitochondria in apoptosis
TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.
Journal ArticleDOI
A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD
Masato Enari,Hideki Sakahira,Hideki Yokoyama,Katsuya Okawa,Akihiro Iwamatsu,Shigekazu Nagata,Shigekazu Nagata +6 more
TL;DR: A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells and seems to function as a chaperone for CAD during its synthesis, remaining complexed with CAD to inhibit its DNase activity.
References
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The Fas Death Factor
Shigekazu Nagata,Pierre Golstein +1 more
TL;DR: Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells.
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Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis
Donald W. Nicholson,Ambereen Ali,Nancy A. Thornberry,John P. Vaillancourt,C K Ding,Michel Gallant,Yves Gareau,Patrick R. Griffin,Marc Labelle,Yuri Lazebnik +9 more
TL;DR: A potent peptide aldehyde inhibitor has been developed and shown to prevent apoptotic events in vitro, suggesting that apopain/CPP32 is important for the initiation of apoptotic cell death.
Journal ArticleDOI
FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.
Marta Muzio,Arul M. Chinnaiyan,Frank C. Kischkel,Karen O'Rourke,Andrej Shevchenko,Jian Ni,Carsten Scaffidi,James D. Bretz,Mei Zhang,Reiner L. Gentz,Matthias Mann,Peter H. Krammer,Marcus E. Peter,Vishva M. Dixit +13 more
TL;DR: This work utilized nano-electrospray tandem mass spectrometry to identify CAP3 and CAP4, components of the CD95 (Fas/APO-1) death-inducing signaling complex, and found a novel 55 kDa protein, designated FLICE, which has homology to both FADD and the ICE/CED-3 family of cysteine proteases.
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An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death
Amer A. Beg,David Baltimore +1 more
TL;DR: Reintroduction of RelA into RelA−/− fibroblasts resulted in enhanced survival, demonstrating that the presence ofrelA is required for protection from TNF-α.
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Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
Rie Watanabe-Fukunaga,Camilynn I. Brannan,Neal G. Copeland,Nancy A. Jenkins,Shigekazu Nagata +4 more
TL;DR: The Ipr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus.