|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0013879,
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0035335,
umls-concept:C0079189,
umls-concept:C0085828,
umls-concept:C0165519,
umls-concept:C0179400,
umls-concept:C0185117,
umls-concept:C0205145,
umls-concept:C0332291,
umls-concept:C0333348,
umls-concept:C0441712,
umls-concept:C1334043,
umls-concept:C1515877,
umls-concept:C1879547,
umls-concept:C1998811,
umls-concept:C2587213,
umls-concept:C2911684
|
|
pubmed:issue |
31
|
|
pubmed:dateCreated |
1993-11-29
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|
pubmed:databankReference |
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|
pubmed:abstractText |
The 92-kDa type IV collagenase (matrix metalloproteinase-9; MMP-9) is frequently expressed in cells showing an invasive nature during physiological and pathological processes, and the expression is strictly controlled by a variety of trans-membrane signals. Binding sites for NF-kB, Sp-1, and AP-1 are reportedly required for induction of MMP-9 gene expression by tumor necrosis factor-alpha or 12-O-tetradecanoylphorbol-13-acetate. Comparison of the sequence of the newly cloned mouse MMP-9 promoter region with our previous human isolate revealed that, in addition to the above mentioned elements, four units of GGGG(T/A)GGGG sequence (GT box) were conserved between the two species. In this study, we have demonstrated that one of the GT boxes located downstream of the AP-1 site is essential along with the AP-1 site for the activation of the promoter by v-Src but not by tumor necrosis factor-alpha or 12-O-tetradecanoylphorbol-13-acetate. Gel mobility-shift assays revealed that binding proteins for retinoblastoma control element, including Sp-1 family protein, can bind specifically to GT boxes. Thus, the v-Src signals to the AP-1 site and to the GT box homologous to retinoblastoma control element acted synergistically in transcriptional activation. These results suggest that certain v-Src-mediated signals are propagated along pathways that are independent of inflammatory cytokines.
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pubmed:language |
eng
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pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
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pubmed:status |
MEDLINE
|
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pubmed:month |
Nov
|
|
pubmed:issn |
0021-9258
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pubmed:author |
|
|
pubmed:issnType |
Print
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|
pubmed:day |
5
|
|
pubmed:volume |
268
|
|
pubmed:geneSymbol |
IGF-II,
MMP-9,
TGF&bgr;1,
TGF&bgr;2,
TGFYbgr;3,
c-fos,
c-myc,
junB,
v-src
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|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
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pubmed:pagination |
23460-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:8226872-Animals,
pubmed-meshheading:8226872-Base Sequence,
pubmed-meshheading:8226872-Collagenases,
pubmed-meshheading:8226872-DNA-Binding Proteins,
pubmed-meshheading:8226872-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:8226872-Genes, src,
pubmed-meshheading:8226872-Humans,
pubmed-meshheading:8226872-Matrix Metalloproteinase 9,
pubmed-meshheading:8226872-Mice,
pubmed-meshheading:8226872-Molecular Sequence Data,
pubmed-meshheading:8226872-Nuclear Proteins,
pubmed-meshheading:8226872-Oncogene Protein pp60(v-src),
pubmed-meshheading:8226872-Promoter Regions, Genetic,
pubmed-meshheading:8226872-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:8226872-RNA, Messenger,
pubmed-meshheading:8226872-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:8226872-Transcriptional Activation
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|
pubmed:year |
1993
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|
pubmed:articleTitle |
v-Src activates the expression of 92-kDa type IV collagenase gene through the AP-1 site and the GT box homologous to retinoblastoma control elements. A mechanism regulating gene expression independent of that by inflammatory cytokines.
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|
pubmed:affiliation |
Department of Molecular Virology and Oncology, Kanazawa University, Japan.
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|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|
