Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
31
pubmed:dateCreated
2002-7-29
pubmed:abstractText
Insulin stimulates malic enzyme (ME)-chloramphenicol acetyltransferase (CAT) and collagenase-1-CAT fusion gene expression in H4IIE cells through identical activator protein-1 (AP-1) motifs. In contrast, insulin and phorbol esters only stimulate collagenase-1-CAT and not ME-CAT fusion gene expression in HeLa cells. The experiments in this article were designed to explore the molecular basis for this differential cell type- and gene-specific regulation. The results highlight the influence of three variables, namely promoter context, AP-1 flanking sequence, and accessory elements that modulate insulin and phorbol ester signaling through the AP-1 motif. Thus, fusion gene transfection and proteolytic clipping gel retardation assays suggest that the AP-1 flanking sequence affects the conformation of AP-1 binding to the collagenase-1 and ME AP-1 motifs such that it selectively binds the latter in a fully activated state. However, this influence of ME AP-1 flanking sequence is dependent on promoter context. Thus, the ME AP-1 motif will mediate both an insulin and phorbol ester response in HeLa cells when introduced into either the collagenase-1 promoter or a specific heterologous promoter. But even in the context of the collagenase-1 promoter, the effects of both insulin and phorbol esters, mediated through the ME AP-1 motif are dependent on accessory factors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Chloramphenicol O-Acetyltransferase, http://linkedlifedata.com/resource/pubmed/chemical/Collagenases, http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Malate Dehydrogenase, http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides, http://linkedlifedata.com/resource/pubmed/chemical/Phorbol Esters, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/beta-Galactosidase, http://linkedlifedata.com/resource/pubmed/chemical/collagenase 1
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27935-44
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12032154-Base Sequence, pubmed-meshheading:12032154-Cell Line, pubmed-meshheading:12032154-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:12032154-Collagenases, pubmed-meshheading:12032154-DNA Primers, pubmed-meshheading:12032154-Gene Expression Regulation, Enzymologic, pubmed-meshheading:12032154-HeLa Cells, pubmed-meshheading:12032154-Humans, pubmed-meshheading:12032154-Insulin, pubmed-meshheading:12032154-Malate Dehydrogenase, pubmed-meshheading:12032154-Mutagenesis, pubmed-meshheading:12032154-Oligodeoxyribonucleotides, pubmed-meshheading:12032154-Phorbol Esters, pubmed-meshheading:12032154-Polymerase Chain Reaction, pubmed-meshheading:12032154-Promoter Regions, Genetic, pubmed-meshheading:12032154-Recombinant Proteins, pubmed-meshheading:12032154-Transcription Factor AP-1, pubmed-meshheading:12032154-Transcription Factors, pubmed-meshheading:12032154-Transfection, pubmed-meshheading:12032154-beta-Galactosidase
pubmed:year
2002
pubmed:articleTitle
Accessory elements, flanking DNA sequence, and promoter context play key roles in determining the efficacy of insulin and phorbol ester signaling through the malic enzyme and collagenase-1 AP-1 motifs.
pubmed:affiliation
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, Tennessee 37232, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.