| pubmed-article:12070137 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0022567 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0010556 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0164786 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0040223 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0728940 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0812228 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0015252 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0332162 | lld:lifeskim |
| pubmed-article:12070137 | lifeskim:mentions | umls-concept:C0040092 | lld:lifeskim |
| pubmed-article:12070137 | pubmed:issue | 36 | lld:pubmed |
| pubmed-article:12070137 | pubmed:dateCreated | 2002-9-2 | lld:pubmed |
| pubmed-article:12070137 | pubmed:abstractText | Insulin-like growth factor-1 (IGF-1) acts as a potent survival factor in numerous cell lines, primarily through activation of the AKT signaling pathway. Although some targets of this pathway have known anti-apoptotic functions, its relationship with the improved survival of cells after exposure to environmental stresses, including UVB, remains largely unclear. We report that in growth factor-deprived keratinocytes, IGF-1 significantly and consistently delayed the onset of UVB-induced apoptosis by >7 h. This delay allowed IGF-1-supplemented keratinocytes to repair significantly more cyclobutane thymine dimers than their growth factor-deprived counterparts. This increase in cyclobutane thymine removal resulted in enhanced survival if the amount of DNA damage was not too high. To increase cell survival after UVB irradiation, IGF-1 supplementation was required only during this initial time period in which extra repair was executed. Finally, we show that IGF-1 mediated this delay in the onset of UVB-induced apoptosis through activation of the AKT signaling pathway. We therefore believe that the AKT signaling pathway increases cell survival after a genotoxic insult such as UVB irradiation not by inhibiting the apoptotic stimulus, but only by postponing the induction of apoptosis, giving the DNA repair mechanism more time to work. | lld:pubmed |
| pubmed-article:12070137 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12070137 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12070137 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12070137 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12070137 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12070137 | pubmed:author | pubmed-author:BouillonRoger... | lld:pubmed |
| pubmed-article:12070137 | pubmed:author | pubmed-author:AgostinisPatr... | lld:pubmed |
| pubmed-article:12070137 | pubmed:author | pubmed-author:DegreefHugoH | lld:pubmed |
| pubmed-article:12070137 | pubmed:author | pubmed-author:GarmynMarjanM | lld:pubmed |
| pubmed-article:12070137 | pubmed:author | pubmed-author:DecraeneDavid... | lld:pubmed |
| pubmed-article:12070137 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12070137 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:12070137 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:12070137 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12070137 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12070137 | pubmed:pagination | 32587-95 | lld:pubmed |
| pubmed-article:12070137 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:12070137 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12070137 | pubmed:articleTitle | Insulin-like growth factor-1-mediated AKT activation postpones the onset of ultraviolet B-induced apoptosis, providing more time for cyclobutane thymine dimer removal in primary human keratinocytes. | lld:pubmed |
| pubmed-article:12070137 | pubmed:affiliation | Department of Dermatology, Faculty of Medicine, Katholieke Universiteit, B-3000 Leuven, Belgium. | lld:pubmed |
| pubmed-article:12070137 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12070137 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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