About: Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence

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About: Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence Goto Sponge NotDistinct Permalink

An Entity of Type : http://linked.opendata.cz/ontology/domain/vavai/Vysledek, within Data Space : linked.opendata.cz associated with source document(s)

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
Description	The telomere-capping complex shelterin protects functional telomeres and prevents the initiation of unwanted DNA-damage-response pathways. At the end of cellular replicative lifespan, uncapped telomeres lose this protective mechanism and DNA-damage signalling pathways are triggered that activate p53 and thereby induce replicative senescence. Here, we identify a signalling pathway involving p53, Siah1 and TRF2. Experimental manipulation of p53 expression demonstrated that p53 induces Siah1 and represses TRF2 protein levels. The p53-dependent ubiquitylation and proteasomal degradation of TRF2 are attributed to the E3 ligase activity of Siah1. Knockdown of Siah1 stabilized TRF2 and delayed the onset of cellular replicative senescence, suggesting a role for Siah1 and TRF2 in p53-regulated senescence. This study reveals that p53, a downstream effector of telomere-initiated damage signalling, also functions upstream of the shelterin complex. The telomere-capping complex shelterin protects functional telomeres and prevents the initiation of unwanted DNA-damage-response pathways. At the end of cellular replicative lifespan, uncapped telomeres lose this protective mechanism and DNA-damage signalling pathways are triggered that activate p53 and thereby induce replicative senescence. Here, we identify a signalling pathway involving p53, Siah1 and TRF2. Experimental manipulation of p53 expression demonstrated that p53 induces Siah1 and represses TRF2 protein levels. The p53-dependent ubiquitylation and proteasomal degradation of TRF2 are attributed to the E3 ligase activity of Siah1. Knockdown of Siah1 stabilized TRF2 and delayed the onset of cellular replicative senescence, suggesting a role for Siah1 and TRF2 in p53-regulated senescence. This study reveals that p53, a downstream effector of telomere-initiated damage signalling, also functions upstream of the shelterin complex. (en)
Title	Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence (en)
skos:prefLabel	Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence (en)
skos:notation	RIV/00209805:_____/10:#0000124!RIV11-GA0-00209805
http://linked.open...avai/riv/aktivita	P
http://linked.open...avai/riv/aktivity	P(GA301/08/1468), P(NS9812)
http://linked.open...iv/cisloPeriodika	12
http://linked.open...vai/riv/dodaniDat	2011
http://linked.open...aciTvurceVysledku	Vojtěšek, Bořivoj
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Masarykův onkologický ústav
http://linked.open...dnocenehoVysledku	280120
http://linked.open...ai/riv/idVysledku	RIV/00209805:_____/10:#0000124
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	p53, telomeres, Siah1, TRF2, senescence (en)
http://linked.open.../riv/klicoveSlovo	TRF2 p53 senescence telomeres Siah1
http://linked.open...odStatuVydavatele	GB - Spojené království Velké Británie a Severního Irska
http://linked.open...ontrolniKodProRIV	[85CB0846942A]
http://linked.open...i/riv/nazevZdroje	Nature cell biology
http://linked.open...in/vavai/riv/obor	FD
http://linked.open...ichTvurcuVysledku	1 (xsd:int)
http://linked.open...cetTvurcuVysledku	9 (xsd:int)
http://linked.open...vavai/riv/projekt	Molecular and cellular consequences of p53 manipulation using heat shock protein inhibitors and E3-ligases. Elucidating the role of ubiquitin-chaperone degradation machinery in cancer and modulating its biochemical functions using targeted chaperone inhibitors
http://linked.open...UplatneniVysledku	2010
http://linked.open...v/svazekPeriodika	12
http://linked.open...iv/tvurceVysledku	Vojtěšek, Bořivoj
http://linked.open...ain/vavai/riv/wos	000284831200012
issn	1465-7392
number of pages	21 (xsd:int)

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