Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2008-12-3
pubmed:abstractText
Cellular senescence is one of the key strategies to suppress expansion of cells with mutations. Senescence is induced in response to genotoxic and oxidative stress. Here we show that the transcription factor Bach1 (BTB and CNC homology 1, basic leucine zipper transcription factor 1), which inhibits oxidative stress-inducible genes, is a crucial negative regulator of oxidative stress-induced cellular senescence. Bach1-deficient murine embryonic fibroblasts showed a propensity to undergo more rapid and profound p53-dependent premature senescence than control wild-type cells in response to oxidative stress. Bach1 formed a complex that contained p53, histone deacetylase 1 and nuclear co-repressor N-coR. Bach1 was recruited to a subset of p53 target genes and contributed to impeding p53 action by promoting histone deacetylation. Because Bach1 is regulated by oxidative stress and heme, our data show that Bach1 connects oxygen metabolism and cellular senescence as a negative regulator of p53.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Bach1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Basic-Leucine Zipper Transcription..., http://linkedlifedata.com/resource/pubmed/chemical/Chromatin, http://linkedlifedata.com/resource/pubmed/chemical/Hdac1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase 1, http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylases, http://linkedlifedata.com/resource/pubmed/chemical/Ncor1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Receptor Co-Repressor 1, http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1545-9985
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1246-54
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19011633-Animals, pubmed-meshheading:19011633-Basic-Leucine Zipper Transcription Factors, pubmed-meshheading:19011633-Cell Aging, pubmed-meshheading:19011633-Cell Count, pubmed-meshheading:19011633-Cell Proliferation, pubmed-meshheading:19011633-Chromatin, pubmed-meshheading:19011633-Fibroblasts, pubmed-meshheading:19011633-Gene Expression Regulation, pubmed-meshheading:19011633-Histone Deacetylase 1, pubmed-meshheading:19011633-Histone Deacetylases, pubmed-meshheading:19011633-Mice, pubmed-meshheading:19011633-Mice, Knockout, pubmed-meshheading:19011633-Nuclear Proteins, pubmed-meshheading:19011633-Nuclear Receptor Co-Repressor 1, pubmed-meshheading:19011633-Oxidative Stress, pubmed-meshheading:19011633-Protein Binding, pubmed-meshheading:19011633-Repressor Proteins, pubmed-meshheading:19011633-Tumor Suppressor Protein p53
pubmed:year
2008
pubmed:articleTitle
Bach1 inhibits oxidative stress-induced cellular senescence by impeding p53 function on chromatin.
pubmed:affiliation
Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't