Linked Life Data

10348347

Source:http://linkedlifedata.com/resource/pubmed/id/10348347

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
1999-6-16
pubmed:abstractText
Transcriptional control of p53 expression participates in the generation of appropriate levels of active p53 in response to mitogenic stimulation. This prompted us to study the role of a putative AP-1 and a NF-kappaB motif in the human p53 promoter for transcriptional regulation. We show that mutation of the AP-1 or the NF-kappaB motif abolishes transcription from the human p53 promoter in HeLa, HepG2 and adenovirus type 5 E1-transformed 293 cells. In comparison, mutation of the previously characterized Myc/Max/USF binding site in the human p53 promoter reduces the transcription rate fivefold. The AP-1 motif in the human p53 promoter binds c-Fos and c-Jun and the NF-kappaB motif binds p50(NF-kappaB) and p65RelA. The cooperative nature of transcriptional activation by these factors was documented by repression of c-fos or NF-kappaB1 translation: Pretreatment of the cells with a c-fos or p50(NF-kappaB1) antisense oligonucleotide suppresses transcription from the human p53 promoter completely. In addition, we show that (a) the level of endogenous p53 mRNA and (b) transcription from the strictly p53-dependent human mdm2 promoter are reduced in the presence of c-fos, c-jun, p50(NF-kappaB1), p65RelA or c-myc antisense oligonucleotides, underscoring the importance of these transcription factors for the expression of functional p53.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2728-38
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Expression of human p53 requires synergistic activation of transcription from the p53 promoter by AP-1, NF-kappaB and Myc/Max.
pubmed:affiliation
Institute of Molecular Biology (Cancer Research), University of Essen, Medical School, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't