| pubmed-article:11566906 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11566906 | lifeskim:mentions | umls-concept:C0034802 | lld:lifeskim |
| pubmed-article:11566906 | lifeskim:mentions | umls-concept:C0390423 | lld:lifeskim |
| pubmed-article:11566906 | lifeskim:mentions | umls-concept:C0214604 | lld:lifeskim |
| pubmed-article:11566906 | lifeskim:mentions | umls-concept:C0040624 | lld:lifeskim |
| pubmed-article:11566906 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:11566906 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11566906 | pubmed:dateCreated | 2001-9-21 | lld:pubmed |
| pubmed-article:11566906 | pubmed:abstractText | Angiotensin (Ang) II has 2 major receptor isoforms, Ang type 1 (AT(1)) and Ang type (AT(2)). AT(1) transphosphorylates epidermal growth factor receptor (EGFR) to activate extracellular signal-regulated kinase (ERK). Although AT(2) was shown to inactivate ERK, the action of AT(2) on EGFR activation remains undefined. Using AT(2)-overexpressing vascular smooth muscle cells from AT(2) transgenic mice, we studied these undefined actions of AT(2). Maximal ERK activity induced by Ang II was increased 1.9- and 2.2-fold by AT(2) inhibition, which was abolished by orthovanadate but not okadaic acid or pertussis toxin. AT(2) inhibited AT(1)-mediated EGFR tyrosine phosphorylation by 63%. The activity of SHP-1 tyrosine phosphatase was significantly upregulated 1 minute after AT(2) stimulation and association of SHP-1 with EGFR was increased, whereas AT(2) failed to tyrosine phosphorylate SHP-1. Stable overexpression of SHP-1-dominant negative mutant completely abolished AT(2)-mediated inhibition of EGFR and ERK activation. AT(1)-mediated c-fos mRNA accumulation was attenuated by 48% by AT(2) stimulation. Induction of fibronectin gene containing an AP-1 responsive element in its 5'-flanking region was decreased by 37% after AT(2) stimulation, corresponding to the results of gel mobility assay with the AP-1 sequence of fibronectin as a probe. These findings suggested that AT(2) inhibits ERK activity by inducing SHP-1 activity, leading to decreases in AP-1 activity and AP-1-regulated gene expression, in which EGFR dephosphorylation plays an important role via association of SHP-1. | lld:pubmed |
| pubmed-article:11566906 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11566906 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11566906 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11566906 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11566906 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11566906 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:11566906 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:MoriYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:NozawaYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:KosakaYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:UchiyamaYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:HasegawaTT | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:MatsubaraHH | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:IwasakaTT | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:HoriuchiMM | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:TsutsumiYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:NahmiasCC | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:FujiyamaSS | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:MasakiHH | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:ShibasakiYY | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:MOEDH KHK | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:IbeKK | lld:pubmed |
| pubmed-article:11566906 | pubmed:author | pubmed-author:TateishiEE | lld:pubmed |
| pubmed-article:11566906 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11566906 | pubmed:volume | 38 | lld:pubmed |
| pubmed-article:11566906 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11566906 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11566906 | pubmed:pagination | 367-72 | lld:pubmed |
| pubmed-article:11566906 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11566906 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11566906 | pubmed:articleTitle | Angiotensin II type 2 receptor inhibits epidermal growth factor receptor transactivation by increasing association of SHP-1 tyrosine phosphatase. | lld:pubmed |
| pubmed-article:11566906 | pubmed:affiliation | Department of Medicine II, Kansai Medical University, Moriguchi, Osaka, Japan. | lld:pubmed |
| pubmed-article:11566906 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11566906 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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