File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: TAp73 depletion accelerates aging through metabolic dysregulation

TitleTAp73 depletion accelerates aging through metabolic dysregulation
Authors
KeywordsAging
P73
Senescence
Mitochondria
Metabolism
ROS
P53
Issue Date2012
Citation
Genes and Development, 2012, v. 26, n. 18, p. 2009-2014 How to Cite?
AbstractAging is associated with impaired scavenging of reactive oxygen species (ROS). Here, we show that TAp73, a p53 family member, protects against aging by regulating mitochondrial activity and preventing ROS accumulation. TAp73-null mice show more pronounced aging with increased oxidative damage and senescence. TAp73 deletion reduces cellular ATP levels, oxygen consumption, and mitochondrial complex IV activity, with increased ROS production and oxidative stress sensitivity. We show that the mitochondrial complex IV subunit cytochrome C oxidase subunit 4 (Cox4i1) is a direct TAp73 target and that Cox4i1 knockdown phenocopies the cellular senescence of TAp73-null cells. Results indicate that TAp73 affects mitochondrial respiration and ROS homeostasis, thus regulating aging. © 2012 by Cold Spring Harbor Laboratory Press.
Persistent Identifierhttp://hdl.handle.net/10722/292726
ISSN
2023 Impact Factor: 7.5
2023 SCImago Journal Rankings: 5.015
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRufini, Alessandro-
dc.contributor.authorNiklison-Chirou, Maria Victoria-
dc.contributor.authorInoue, Satoshi-
dc.contributor.authorTomasini, Richard-
dc.contributor.authorHarris, Isaac S.-
dc.contributor.authorMarino, Arianna-
dc.contributor.authorFederici, Massimo-
dc.contributor.authorDinsdale, David-
dc.contributor.authorKnight, Richard A.-
dc.contributor.authorMelino, Gerry-
dc.contributor.authorMak, Tak Wah-
dc.date.accessioned2020-11-17T14:57:05Z-
dc.date.available2020-11-17T14:57:05Z-
dc.date.issued2012-
dc.identifier.citationGenes and Development, 2012, v. 26, n. 18, p. 2009-2014-
dc.identifier.issn0890-9369-
dc.identifier.urihttp://hdl.handle.net/10722/292726-
dc.description.abstractAging is associated with impaired scavenging of reactive oxygen species (ROS). Here, we show that TAp73, a p53 family member, protects against aging by regulating mitochondrial activity and preventing ROS accumulation. TAp73-null mice show more pronounced aging with increased oxidative damage and senescence. TAp73 deletion reduces cellular ATP levels, oxygen consumption, and mitochondrial complex IV activity, with increased ROS production and oxidative stress sensitivity. We show that the mitochondrial complex IV subunit cytochrome C oxidase subunit 4 (Cox4i1) is a direct TAp73 target and that Cox4i1 knockdown phenocopies the cellular senescence of TAp73-null cells. Results indicate that TAp73 affects mitochondrial respiration and ROS homeostasis, thus regulating aging. © 2012 by Cold Spring Harbor Laboratory Press.-
dc.languageeng-
dc.relation.ispartofGenes and Development-
dc.subjectAging-
dc.subjectP73-
dc.subjectSenescence-
dc.subjectMitochondria-
dc.subjectMetabolism-
dc.subjectROS-
dc.subjectP53-
dc.titleTAp73 depletion accelerates aging through metabolic dysregulation-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1101/gad.197640.112-
dc.identifier.pmid22987635-
dc.identifier.pmcidPMC3444727-
dc.identifier.scopuseid_2-s2.0-84866497949-
dc.identifier.volume26-
dc.identifier.issue18-
dc.identifier.spage2009-
dc.identifier.epage2014-
dc.identifier.eissn1549-5477-
dc.identifier.isiWOS:000308975900003-
dc.identifier.issnl0890-9369-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats