Source:http://linkedlifedata.com/resource/pubmed/id/20473297
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-6-2
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pubmed:abstractText |
Adult stem cells (SCs) are at high risk of accumulating deleterious mutations because they reside and self-renew in adult tissues for extended periods. Little is known about how adult SCs sense and respond to DNA damage within their natural niche. Here, using mouse epidermis as a model, we define the functional consequences and the molecular mechanisms by which adult SCs respond to DNA damage. We show that multipotent hair-follicle-bulge SCs have two important mechanisms for increasing their resistance to DNA-damage-induced cell death: higher expression of the anti-apoptotic gene Bcl-2 and transient stabilization of p53 after DNA damage in bulge SCs. The attenuated p53 activation is the consequence of a faster DNA repair activity, mediated by a higher non-homologous end joining (NHEJ) activity, induced by the key protein DNA-PK. Because NHEJ is an error-prone mechanism, this novel characteristic of adult SCs may have important implications in cancer development and ageing.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1476-4679
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pubmed:author |
pubmed-author:BlanpainCédricC,
pubmed-author:CandiAurélieA,
pubmed-author:DahlEllenE,
pubmed-author:De ClercqSarahS,
pubmed-author:DeneckerGeertruiG,
pubmed-author:LapougeGaelleG,
pubmed-author:MarineJean-ChristopheJC,
pubmed-author:MascréGuilhemG,
pubmed-author:SemeraroClaudioC,
pubmed-author:SotiropoulouPanagiota APA,
pubmed-author:YoussefKhalil KassKK
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pubmed:issnType |
Electronic
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
572-82
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pubmed:meshHeading |
pubmed-meshheading:20473297-Adult,
pubmed-meshheading:20473297-Aging,
pubmed-meshheading:20473297-Animals,
pubmed-meshheading:20473297-Biochemical Processes,
pubmed-meshheading:20473297-Cell Death,
pubmed-meshheading:20473297-DNA,
pubmed-meshheading:20473297-DNA Damage,
pubmed-meshheading:20473297-DNA Repair,
pubmed-meshheading:20473297-Epidermis,
pubmed-meshheading:20473297-Hair Follicle,
pubmed-meshheading:20473297-Humans,
pubmed-meshheading:20473297-Mice,
pubmed-meshheading:20473297-Mice, Inbred BALB C,
pubmed-meshheading:20473297-Mice, Inbred C57BL,
pubmed-meshheading:20473297-Mice, Inbred Strains,
pubmed-meshheading:20473297-Mice, Knockout,
pubmed-meshheading:20473297-Mice, SCID,
pubmed-meshheading:20473297-Multipotent Stem Cells,
pubmed-meshheading:20473297-Stem Cells,
pubmed-meshheading:20473297-Tumor Suppressor Protein p53
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pubmed:year |
2010
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pubmed:articleTitle |
Bcl-2 and accelerated DNA repair mediates resistance of hair follicle bulge stem cells to DNA-damage-induced cell death.
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pubmed:affiliation |
Interdisciplinary Research Institute (IRIBHM), Université Libre de Bruxelles (ULB), 808, route de Lennik, BatC, C6-130, 1070 Brussels, Belgium.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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