@article {2997,
	title = {Translocation of C. elegans CED-4 to nuclear membranes during programmed cell death.},
	journal = {Science},
	volume = {287},
	number = {5457},
	year = {2000},
	month = {2000 Feb 25},
	pages = {1485-9},
	abstract = {The Caenorhabditis elegans Bcl-2-like protein CED-9 prevents programmed cell death by antagonizing the Apaf-1-like cell-death activator CED-4. Endogenous CED-9 and CED-4 proteins localized to mitochondria in wild-type embryos, in which most cells survive. By contrast, in embryos in which cells had been induced to die, CED-4 assumed a perinuclear localization. CED-4 translocation induced by the cell-death activator EGL-1 was blocked by a gain-of-function mutation in ced-9 but was not dependent on ced-3 function, suggesting that CED-4 translocation precedes caspase activation and the execution phase of programmed cell death. Thus, a change in the subcellular localization of CED-4 may drive programmed cell death.},
	keywords = {Amino Acid Substitution, Animals, Animals, Genetically Modified, Apoptosis, Apoptosis Regulatory Proteins, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Calcium-Binding Proteins, Caspases, Cysteine Endopeptidases, Genes, Helminth, Helminth Proteins, Immunohistochemistry, Mitochondria, Mutation, Nuclear Envelope, Phenotype, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Repressor Proteins},
	issn = {0036-8075},
	author = {Chen, F and Hersh, B M and Conradt, B and Zhou, Z and Riemer, D and Gruenbaum, Y and Horvitz, H R}
}
