FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis

被引:787
作者
Yeh, WC
de la Pompa, JL
McCurrach, ME
Shu, HB
Elia, AJ
Shahinian, A
Ng, M
Wakeham, A
Khoo, W
Mitchell, K
El-Deiry, WS
Lowe, SW
Goeddel, DV
Mak, TW
机构
[1] Univ Toronto, Amgen Inst, Toronto, ON M5G 2C1, Canada
[2] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2C1, Canada
[3] Univ Toronto, Dept Immunol, Toronto, ON M5G 2C1, Canada
[4] Ontario Canc Inst, Toronto, ON M5G 2C1, Canada
[5] Cold Spring Harbor Labs, Cold Spring Harbor, NY 11724 USA
[6] Tularik, S San Francisco, CA 94080 USA
[7] Univ Penn, Sch Med, Howard Hughes Med Inst, Philadelphia, PA 19104 USA
关键词
D O I
10.1126/science.279.5358.1954
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1954 / 1958
页数:5
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