| pubmed-article:19197340 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C0231337 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C1418626 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19197340 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19197340 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19197340 | pubmed:dateCreated | 2009-3-3 | lld:pubmed |
| pubmed-article:19197340 | pubmed:abstractText | Senescence is a stable proliferative arrest induced by various stresses such as telomere erosion, oncogenic or oxidative stress. Compelling evidence suggests that it acts as a barrier against tumour development. Describing new mechanisms that favour an escape from senescence can thus reveal new insights into tumorigenesis. To identify new genes controlling the senescence programme, we performed a loss-of-function genetic screen in primary human fibroblasts. We report that knockdown of the M-type receptor PLA2R (phospholipase A2 receptor) prevents the onset of replicative senescence and diminishes stress-induced senescence. Interestingly, expression of PLA2R increases during replicative senescence, and its ectopic expression results in premature senescence. We show that PLA2R regulates senescence in a reactive oxygen species-DNA damage-p53-dependent manner. Taken together, our study identifies PLA2R as a potential new tumour suppressor gene crucial in the induction of cellular senescence through the activation of the p53 pathway. | lld:pubmed |
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| pubmed-article:19197340 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19197340 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19197340 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19197340 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19197340 | pubmed:issn | 1469-3178 | lld:pubmed |
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| pubmed-article:19197340 | pubmed:author | pubmed-author:BernardDavidD | lld:pubmed |
| pubmed-article:19197340 | pubmed:author | pubmed-author:GilJesusJ | lld:pubmed |
| pubmed-article:19197340 | pubmed:author | pubmed-author:AugertArnaudA | lld:pubmed |
| pubmed-article:19197340 | pubmed:author | pubmed-author:PayréChristin... | lld:pubmed |
| pubmed-article:19197340 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19197340 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:19197340 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19197340 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19197340 | pubmed:pagination | 271-7 | lld:pubmed |
| pubmed-article:19197340 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
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| pubmed-article:19197340 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19197340 | pubmed:articleTitle | The M-type receptor PLA2R regulates senescence through the p53 pathway. | lld:pubmed |
| pubmed-article:19197340 | pubmed:affiliation | UMR 8161, Institut de Biologie de Lille, CNRS/Universités de Lille 1 et 2/Institut Pasteur de Lille, IFR 142, 59021 Lille, France. | lld:pubmed |
| pubmed-article:19197340 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19197340 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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