| pubmed-article:16239930 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16239930 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16239930 | lifeskim:mentions | umls-concept:C0013936 | lld:lifeskim |
| pubmed-article:16239930 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16239930 | pubmed:dateCreated | 2006-6-16 | lld:pubmed |
| pubmed-article:16239930 | pubmed:abstractText | The mitochondrial protein, endonuclease G (EndoG), is one of the endonucleases implicated in DNA fragmentation during apoptosis. It has been shown to translocate from the mitochondria to the nucleus upon cell death stimuli. These observations suggest that EndoG is a mitochondrial cell death effector, and that it possibly acts as a cell death nuclease, similar to DNA fragmentation factor. To better understand the role of EndoG in development and apoptosis, we generated EndoG null mice by homologous gene targeting without disruption of D2Wsu81e. EndoG null mice are viable and develop to adulthood with no obvious abnormalities. Fibroblasts generated from the EndoG null mice show no difference in susceptibility when induced to die by a variety of intrinsic and extrinsic apoptotic stimuli. Additionally, EndoG null mice are equally sensitive to excitotoxic stress. These data suggest that EndoG is not essential for early embryogenesis and apoptosis. | lld:pubmed |
| pubmed-article:16239930 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16239930 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16239930 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16239930 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16239930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16239930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16239930 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16239930 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:16239930 | pubmed:issn | 1350-9047 | lld:pubmed |
| pubmed-article:16239930 | pubmed:author | pubmed-author:SasakiMM | lld:pubmed |
| pubmed-article:16239930 | pubmed:author | pubmed-author:DawsonT MTM | lld:pubmed |
| pubmed-article:16239930 | pubmed:author | pubmed-author:DawsonV LVL | lld:pubmed |
| pubmed-article:16239930 | pubmed:author | pubmed-author:OmiJJ | lld:pubmed |
| pubmed-article:16239930 | pubmed:author | pubmed-author:DavidK KKK | lld:pubmed |
| pubmed-article:16239930 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16239930 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:16239930 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16239930 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16239930 | pubmed:pagination | 1147-55 | lld:pubmed |
| pubmed-article:16239930 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:16239930 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16239930 | pubmed:articleTitle | EndoG is dispensable in embryogenesis and apoptosis. | lld:pubmed |
| pubmed-article:16239930 | pubmed:affiliation | Institute for Cell Engineering Program in Neuroregeneration and Repair, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. | lld:pubmed |
| pubmed-article:16239930 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16239930 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16239930 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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