Linked Life Data

10978511

Source:http://linkedlifedata.com/resource/pubmed/id/10978511

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-11-7
pubmed:abstractText
STAT3 is involved in the signal transduction activated by various cytokines and growth factors. We found that the STAT3 gene is overexpressed in cisplatin-resistant cells. We isolated a genomic fragment containing the 5'-portion of the human STAT3 gene using a bubble PCR method. Using the bubble PCR product as a probe, one genomic clone was isolated. The nucleotide sequence of the first exon and the 1800 base pairs (bps) preceding it was determined. The promoter region of the human STAT3 gene is highly homologous to the corresponding region of the mouse STAT3 gene; several potential factor binding sites such as CRE/ATF, SBE, and GC boxes are also well conserved between human and mouse. A transient expression assay using the luciferase reporter gene showed that the sequence from -403 to +102 possesses maximal promoter activity, and transcription of the STAT3 gene was significantly higher in cisplatin-resistant cells than in parental cisplatin-sensitive cells. Deletion of the region between -261 and -167 resulted in significant loss of promoter activity in both parental and cisplatin-resistant cells. In vivo footprint analysis revealed several protein bindings; however, no significant differences were observed between drug-sensitive and drug-resistant cells. MNase digestion revealed that several open or active nucleosomes were only detected in cisplatin-resistant cells. These results suggest that STAT3 promoter function in a highly structured chromatin environment requires a complex interaction of several transcriptional factors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
1493
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-100
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10978511-Base Sequence, pubmed-meshheading:10978511-Binding Sites, pubmed-meshheading:10978511-Chromatin, pubmed-meshheading:10978511-Cisplatin, pubmed-meshheading:10978511-Cloning, Molecular, pubmed-meshheading:10978511-DNA Footprinting, pubmed-meshheading:10978511-DNA-Binding Proteins, pubmed-meshheading:10978511-Drug Resistance, pubmed-meshheading:10978511-Humans, pubmed-meshheading:10978511-Micrococcal Nuclease, pubmed-meshheading:10978511-Molecular Sequence Data, pubmed-meshheading:10978511-Polymerase Chain Reaction, pubmed-meshheading:10978511-Promoter Regions, Genetic, pubmed-meshheading:10978511-RNA, Messenger, pubmed-meshheading:10978511-Restriction Mapping, pubmed-meshheading:10978511-STAT3 Transcription Factor, pubmed-meshheading:10978511-Trans-Activators, pubmed-meshheading:10978511-Transcription, Genetic, pubmed-meshheading:10978511-Tumor Cells, Cultured, pubmed-meshheading:10978511-Up-Regulation
pubmed:year
2000
pubmed:articleTitle
Structure and functional analysis of the human STAT3 gene promoter: alteration of chromatin structure as a possible mechanism for the upregulation in cisplatin-resistant cells.
pubmed:affiliation
Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka Yahatanishi-ku , Kitakyushu, Fukuoka 807-8555, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't