| pubmed-article:17889652 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17889652 | lifeskim:mentions | umls-concept:C0007620 | lld:lifeskim |
| pubmed-article:17889652 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:17889652 | lifeskim:mentions | umls-concept:C0027270 | lld:lifeskim |
| pubmed-article:17889652 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:17889652 | lifeskim:mentions | umls-concept:C1609990 | lld:lifeskim |
| pubmed-article:17889652 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17889652 | pubmed:dateCreated | 2007-9-24 | lld:pubmed |
| pubmed-article:17889652 | pubmed:abstractText | A major cause of cell death caused by genotoxic stress is thought to be due to the depletion of NAD(+) from the nucleus and the cytoplasm. Here we show that NAD(+) levels in mitochondria remain at physiological levels following genotoxic stress and can maintain cell viability even when nuclear and cytoplasmic pools of NAD(+) are depleted. Rodents fasted for 48 hr show increased levels of the NAD(+) biosynthetic enzyme Nampt and a concomitant increase in mitochondrial NAD(+). Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4. We discuss the relevance of these findings to understanding how nutrition modulates physiology and to the evolution of apoptosis. | lld:pubmed |
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| pubmed-article:17889652 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17889652 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17889652 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:17889652 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:PerezEvelynE | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:SinclairDavid... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:BohrVilhelm... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:RosenzweigAnt... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:YangHongyingH | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:MatsuiTakashi... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:SauveAnthony... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:YangTianleT | lld:pubmed |
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| pubmed-article:17889652 | pubmed:author | pubmed-author:LammingDudley... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:BaurJoseph... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:Souza-PintoNa... | lld:pubmed |
| pubmed-article:17889652 | pubmed:author | pubmed-author:CarmonaJuan... | lld:pubmed |
| pubmed-article:17889652 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17889652 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:17889652 | pubmed:volume | 130 | lld:pubmed |
| pubmed-article:17889652 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17889652 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17889652 | pubmed:pagination | 1095-107 | lld:pubmed |
| pubmed-article:17889652 | pubmed:dateRevised | 2011-2-14 | lld:pubmed |
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| pubmed-article:17889652 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17889652 | pubmed:articleTitle | Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. | lld:pubmed |
| pubmed-article:17889652 | pubmed:affiliation | Department of Pathology, Paul F. Glenn Laboratories, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:17889652 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17889652 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17889652 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| pubmed-article:17889652 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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