2003
DOI: 10.1073/pnas.2636393100
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Abstract: Endonuclease G (EndoG) is a nuclear-encoded mitochondrial protein reported to be important for both nuclear DNA fragmentation during apoptosis and mitochondrial DNA replication. To evaluate the in vivo function of EndoG, we have investigated the effects of EndoG deficiency in cells and mice. We found that EndoG homozygous mutant embryos die between embryonic days 2.5 and 3.5. Mitochondrial DNA copy numbers in ovulated oocytes from EndoG heterozygous mutant and wild-type mice are similar, suggesting that EndoG … Show more

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Cited by 82 publications
(62 citation statements)
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“…embryos 30 and during the four-cell embryo stage. 31 Our results differ from a report of an EndoG knockout describing embryonic lethality 17 in which they targeted all of the exons of EndoG including a substantial portion of D2Wsu81e (five of the 10 exons were deleted). Thus, the original description of early embryonic lethality in EndoG knockout mice is due to the inadvertent double gene disruption of EndoG and D2Wsu81e.…”
Section: Discussioncontrasting
confidence: 89%
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“…embryos 30 and during the four-cell embryo stage. 31 Our results differ from a report of an EndoG knockout describing embryonic lethality 17 in which they targeted all of the exons of EndoG including a substantial portion of D2Wsu81e (five of the 10 exons were deleted). Thus, the original description of early embryonic lethality in EndoG knockout mice is due to the inadvertent double gene disruption of EndoG and D2Wsu81e.…”
Section: Discussioncontrasting
confidence: 89%
“…The EndoG null mice are viable and develop to adulthood with no obvious abnormalities. This is in contrast with a previous report describing embryonic lethality in EndoG null mice, 17 but agrees with a recent report describing viability and lack of obvious abnormalities in EndoG null mice. 18 We extend the latter study by treating mouse embryonic fibroblasts with different cell death stimuli and by subjecting EndoG null mice to excitotoxicity.…”
Section: Introductionsupporting
confidence: 84%
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“…The loss of EndoG activity in C.elegans resulted in increased cell survival [8]. It was recently demonstrated that homozygous EndoG−/− knockout mice (129 x C57 background) are not viable, which suggests the great importance of this enzyme for apoptosis during early development [42]. There is a possibility that other factors may affect the role of EndoG in embryogenesis because EndoG−/− knockout mice in C57 background was viable [43].…”
Section: Discussionmentioning
confidence: 99%
“…Known as apoptogenic proteins, these released proteins include cytochrome c (Yang et al, 1997), AIF (Susin et al, 1996), HtrA2/Omi (Suzuki et al, 2001), SMAC/Diablo (Du et al, 2000) and EndoG (Li et al, 2001b;Zhang et al, 2003a) of which cytochrome c has been the most intensively studied. Upon intrinsic apoptotic stimulation, cytochrome c is released into the cytosol where it triggers the formation of the apoptosome, a multimeric molecule comprising of apoptotic protease activating factor-1 (Apaf-1), ATP or dATP and cytochrome c (Cain et al, 2002).…”
Section: Introductionmentioning
confidence: 99%