Interaction between the C-elegans cell-death regulators CED-9 and CED-4

被引:258
作者
Spector, MS
Desnoyers, S
Hoeppner, DJ
Hengartner, MO
机构
[1] COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724
[2] SUNY STONY BROOK,DEPT MOL MICROBIOL,GRAD PROGRAM GENET,STONY BROOK,NY 11794
关键词
D O I
10.1038/385653a0
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
Programmed cell death (apoptosis) is an evolutionarily conserved process used by multicellular organisms to eliminate cells that are not needed or are potentially detrimental to the organism(1,2). Members of the Bcl-2 family of mammalian proteins are intimately involved in the regulation of apoptosis, but, their precise mechanism of action remains unresolved(3-5). In Caenorhabditis elegans, the Bcl-2 homologue CED-9 prevents cell death by antagonizing the death-promoting activities of CED-3, a member of the Caspase family of death proteases, and of CED-4, a protein with no known mammalian homologue(6-9). Here we show that CED-9 interacts physically with CED-4. Mutations that reduce or eliminate CED-9 activity also disrupt its ability to bind CED-4, suggesting that this interaction is important for CED-9 function. Thus, CED-9 might control C. elegans cell death by binding to and regulating CED-4 activity. We propose that mammalian Bcl-2 family members might control apoptosis in a similar way through interaction and regulation of CED-4 homologues or analogues.
引用
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页码:653 / 656
页数:4
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