FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
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DOI：
10.1126/science.279.5358.1954
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发表时间：
1998-03-20
期刊：
影响因子：
56.9
通讯作者：
Mak, TW
中科院分区：
文献类型：
--
作者：
Yeh, WC;de la Pompa, JL;Mak, TW
FADD（也称为Mort-1）是细胞死亡受体CD 95（也称为Fas）下游的信号转导子，CD 95、肿瘤坏死因子受体1（TNFR-1）和死亡受体3（DR 3）在FADD缺陷的胚胎成纤维细胞中不诱导凋亡，而DR 4、癌基因E1 A和c-myc和化疗剂阿霉素诱导凋亡。FADD基因缺失的小鼠在胚胎发育的第11.5天后不能存活，这些小鼠表现出心力衰竭和腹部出血的迹象。显示FADD无效突变细胞对心脏的高贡献的嵌合胚胎再现FADD缺陷突变体的表型。因此，不仅死亡受体，而且与发育程序偶联的受体也可以使用FADD进行信号传导。
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.