Linked Life Data

20149781

Source:http://linkedlifedata.com/resource/pubmed/id/20149781

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-3-8
pubmed:abstractText
CD151 plays an important role in liver cancer metastasis. The mechanism on how CD151 is expressed remains unclear. Here we have identified SP1 is a protein functioning in constitutive activation of CD151. Applying a PCR-based chromatin accessibility assay, an open chromatin conformation was discovered localized around the transcription start site of the CD151 gene. Deletion constructs of the 5' flanking region were fused to a luciferase reporter gene. After transient transfection in HepG2 and Hep3B cells, a minimal region -171/-53 bearing three SP1-binding sites was identified as the core promoter. Results obtained from electrophoretic mobility shift and chromatin immunoprecipitation assays demonstrated that SP1 is bound to the core promoter. Deletion of SP1 consensus sequence resulted in the total loss of the promoter activity. Moreover, knockdown of SP1 reduced both CD151 promoter activity and chromatin accessibility. Conclusively, SP1 is pivotal to CD151 transcription partly via the construction of a local open chromatin configuration across the promoter.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1090-2104
pubmed:author
pubmed:copyrightInfo
2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
5
pubmed:volume
393
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
291-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
SP1 is required for basal activation and chromatin accessibility of CD151 promoter in liver cancer cells.
pubmed:affiliation
Department of Laboratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't