Abstract
The critical point at which apoptosis becomes irreversible and how cells attain an anti-apoptotic state remain unknown. Here, we report that apoptotic cells undergoing early-stage dynamic membrane blebbing revive. We examined this phenomenon in cell lines that stably express 2DED2DD, a modified FADD produced by fusing the tandem death effector domains (DEDs) and tandem death domains (DDs). Induction of apoptosis caused rapid blebbing. Eight hours later, most cells shrunk while some detached from the flask. Twenty-four hours later, when activated caspase 3 decreased, more than half the cells revived and appeared normal, probably due to the induction of unidentified anti-apoptotic proteins.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Chloromethyl Ketones / pharmacology
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Apoptosis / genetics
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Apoptosis / physiology*
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CASP8 and FADD-Like Apoptosis Regulating Protein / genetics
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CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism
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CASP8 and FADD-Like Apoptosis Regulating Protein / physiology
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Caspase 3 / metabolism
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Caspase Inhibitors
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Cell Line
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Cell Membrane / metabolism*
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Fas-Associated Death Domain Protein / genetics
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Fas-Associated Death Domain Protein / metabolism
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Fas-Associated Death Domain Protein / physiology
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Humans
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Immunoblotting
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Microscopy, Fluorescence
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Microscopy, Phase-Contrast
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Oligopeptides / pharmacology
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Proto-Oncogene Proteins c-bcl-2 / physiology
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Time Factors
Substances
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Amino Acid Chloromethyl Ketones
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CASP8 and FADD-Like Apoptosis Regulating Protein
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Caspase Inhibitors
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Fas-Associated Death Domain Protein
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Oligopeptides
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Proto-Oncogene Proteins c-bcl-2
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acetyl-aspartyl-glutamyl-valyl-aspartal
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benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
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Caspase 3