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Science 20 March 1998: Vol. 279. no. 5358, pp. 1954 - 1958 DOI: 10.1126/science.279.5358.1954
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Reports
FADD: Essential for Embryo Development and Signaling from Some, But Not All, Inducers of Apoptosis
Wen-Chen Yeh,
José Luis de la Pompa,
Mila E. McCurrach,
Hong-Bing Shu,
Andrew J. Elia,
Arda Shahinian,
Michelle Ng,
Andrew Wakeham,
Wilson Khoo,
Kyran Mitchell,
Wafik S. El-Deiry,
Scott W. Lowe,
David V. Goeddel,
Tak W. Mak
*
FADD (also known as Mort-1) is a signal transducer downstream of
cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor
receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not
induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4,
oncogenes E1A and c-myc, and chemotherapeutic
agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of
cardiac failure and abdominal hemorrhage. Chimeric embryos showing a
high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death
receptors, but also receptors that couple to developmental programs,
may use FADD for signaling.
W.-C. Yeh, J. L. de la Pompa, A. J. Elia, A. Shahinian,
M. Ng, A. Wakeham, W. Khoo, T. W. Mak, Amgen Institute,
Departments of Medical Biophysics and Immunology, University of
Toronto, and Ontario Cancer Institute, 610 University Avenue, Toronto,
Ontario M5G 2C1, Canada.
M. E. McCurrach and S. W. Lowe, Cold Spring Harbor
Laboratories, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.
H.-B. Shu and D. V. Goeddel, Tularik, 2 Corporate Drive, South San
Francisco, CA 94080, USA.
K. Mitchell and W. S. El-Deiry, Howard Hughes Medical Institute,
University of Pennsylvania School of Medicine CRB 437A, Philadelphia,
PA 19104, USA.
*
To whom correspondence should be addressed. E-mail:
t.mak{at}oci.utoronto.ca
Read the Full Text
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23, 8526-8531
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- The Apoptosis-Necrosis Continuum: Insights from Genetically Altered Mice.
- C. J. Zeiss (2003)
Vet. Pathol.
40, 481-495
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- Tracking death dealing by Fas and TRAIL in lymphatic neoplastic disorders: pathways, targets, and therapeutic tools.
- R. Greil, G. Anether, K. Johrer, and I. Tinhofer (2003)
J. Leukoc. Biol.
74, 311-330
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- Fas-associated Death Domain Protein and Caspase-8 Are Not Recruited to the Tumor Necrosis Factor Receptor 1 Signaling Complex during Tumor Necrosis Factor-induced Apoptosis.
- N. Harper, M. Hughes, M. MacFarlane, and G. M. Cohen (2003)
J. Biol. Chem.
278, 25534-25541
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- The Requirements for Fas-Associated Death Domain Signaling in Mature T Cell Activation and Survival.
- D. R. Beisner, I. H. Chu, A. F. Arechiga, S. M. Hedrick, and C. M. Walsh (2003)
J. Immunol.
171, 247-256
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- Role of SODD in Regulation of Tumor Necrosis Factor Responses.
- H. Takada, N.-J. Chen, C. Mirtsos, S. Suzuki, N. Suzuki, A. Wakeham, T. W. Mak, and W.-C. Yeh (2003)
Mol. Cell. Biol.
23, 4026-4033
| Abstract »
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- c-Jun NH2-Terminal Kinase Is Essential for the Regulation of AP-1 by Tumor Necrosis Factor.
- J.-J. Ventura, N. J. Kennedy, J. A. Lamb, R. A. Flavell, and R. J. Davis (2003)
Mol. Cell. Biol.
23, 2871-2882
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- Caspases signal not only apoptosis but also antigen-induced activation in cells of the immune system.
- K. Newton and A. Strasser (2003)
Genes & Dev.
17, 819-825
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- Dexamethasone-induced apoptosis of thymocytes: role of glucocorticoid receptor-associated Src kinase and caspase-8 activation.
- M. C. Marchetti, B. Di Marco, G. Cifone, G. Migliorati, and C. Riccardi (2003)
Blood
101, 585-593
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- LF 15-0195 immunosuppressive agent enhances activation-induced T-cell death by facilitating caspase-8 and caspase-10 activation at the DISC level.
- P. Ducoroy, O. Micheau, S. Perruche, L. Dubrez-Daloz, D. de Fornel, P. Dutartre, P. Saas, and E. Solary (2003)
Blood
101, 194-201
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- Hepatocyte Fas-associating Death Domain Protein/Mediator of Receptor-induced Toxicity (FADD/MORT1) Levels Increase in Response to Pro-apoptotic Stimuli.
- P. K. M. Kim, Y. Wang, A. Gambotto, Y.-M. Kim, R. Weller, B. S. Zuckerbraun, Y. Hua, S. C. Watkins, and T. R. Billiar (2002)
J. Biol. Chem.
277, 38855-38862
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- Tumor Necrosis Factor Induces Apoptosis in Hepatoma Cells by Increasing Ca2+ Release from the Endoplasmic Reticulum and Suppressing Bcl-2 Expression.
- B.-C. Kim, H.-T. Kim, M. Mamura, I. S. Ambudkar, K.-S. Choi, and S.-J. Kim (2002)
J. Biol. Chem.
277, 31381-31389
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- Resistance to Fas-mediated apoptosis in human lung fibroblast.
- T. Tanaka, M. Yoshimi, T. Maeyama, N. Hagimoto, K. Kuwano, and N. Hara (2002)
Eur. Respir. J.
20, 359-368
| Abstract »
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- c-Myc Controls Proliferation Versus Differentiation in Human Pancreatic Endocrine Cells.
- C. Demeterco, P. Itkin-Ansari, B. Tyrberg, L. P. Ford, R. A. Jarvis, and F. Levine (2002)
J. Clin. Endocrinol. Metab.
87, 3475-3485
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- Nuclear and cytoplasmic shuttling of TRADD induces apoptosis via different mechanisms.
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J. Cell Biol.
157, 975-984
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- Inactivating mutations of CASP10 gene in non-Hodgkin lymphomas.
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Blood
99, 4094-4099
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- A Novel Zinc Finger Protein Interacts with Receptor-interacting Protein (RIP) and Inhibits Tumor Necrosis Factor (TNF)- and IL1-induced NF-kappa B Activation.
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J. Biol. Chem.
277, 15985-15991
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- The procaspase-8 isoform, procaspase-8L, recruited to the BAP31 complex at the endoplasmic reticulum.
- D. G. Breckenridge, M. Nguyen, S. Kuppig, M. Reth, and G. C. Shore (2002)
PNAS
99, 4331-4336
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- Paclitaxel Triggers Cell Death Primarily via Caspase-independent Routes in the Non-Small Cell Lung Cancer Cell Line NCI-H460.
- C. Huisman, C. G. Ferreira, L. E. Broker, J. A. Rodriguez, E. F. Smit, P. E. Postmus, F. A. E. Kruyt, and G. Giaccone (2002)
Clin. Cancer Res.
8, 596-606
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- Binding of FADD and Caspase-8 to Molluscum Contagiosum Virus MC159 v-FLIP Is Not Sufficient for Its Antiapoptotic Function.
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J. Virol.
76, 697-706
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- Molecular Cross-talk between the TRAIL and Interferon Signaling Pathways.
- C. Kumar-Sinha, S. Varambally, A. Sreekumar, and A. M. Chinnaiyan (2002)
J. Biol. Chem.
277, 575-585
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- FLICE-Inhibitory Proteins: Regulators of Death Receptor-Mediated Apoptosis.
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Mol. Cell. Biol.
21, 8247-8254
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- Fas Ligand Engagement of Resident Peritoneal Macrophages In Vivo Induces Apoptosis and the Production of Neutrophil Chemotactic Factors.
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J. Immunol.
167, 6217-6224
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