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| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0227525 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0003018 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C1522642 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0529330 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C0599281 | lld:lifeskim |
| pubmed-article:11875120 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11875120 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11875120 | pubmed:dateCreated | 2002-3-4 | lld:pubmed |
| pubmed-article:11875120 | pubmed:abstractText | The agonist-induced internalization of several G protein-coupled receptors is an obligatory requirement for their activation of MAPKs. Studies on the relationship between endocytosis of the angiotensin II (Ang II) type 1 receptor (AT1-R) and Ang II-induced ERK1/2 activation were performed in clone 9 (C9) rat hepatic cells treated with inhibitors of endocytosis [sucrose, phenylarsine oxide (PAO), and concanavalin A]. Although Ang II-induced endocytosis of the AT1-R was prevented by sucrose and PAO, and was partially inhibited by concanavalin A, there was no impairment of Ang II-induced ERK activation. However, the specific epidermal growth factor receptor (EGF-R) kinase inhibitor, AG1478, abolished Ang II-induced activation of ERK1/2. Sucrose and PAO also inhibited EGFinduced internalization of the EGF-R in C9 cells, and the inability of these agents to impair EGF-induced ERK activation suggested that the latter is also independent of receptor endocytosis. In COS-7 cells transiently expressing the rat AT1A-R, Ang II also caused ERK activation through EGF-R transactivation. Furthermore, a mutant AT1A-R with truncated carboxyl terminus and impaired internalization retained full ability to activate ERK1/2 in response to Ang II stimulation. These findings demonstrate that Ang II-induced ERK1/2 activation in C9 hepatocytes is independent of both AT1-R and EGF-R endocytosis and is mediated by transactivation of the EGF-R. | lld:pubmed |
| pubmed-article:11875120 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11875120 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11875120 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11875120 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11875120 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:11875120 | pubmed:issn | 0888-8809 | lld:pubmed |
| pubmed-article:11875120 | pubmed:author | pubmed-author:ShahBukhtiar... | lld:pubmed |
| pubmed-article:11875120 | pubmed:author | pubmed-author:CattKevin JKJ | lld:pubmed |
| pubmed-article:11875120 | pubmed:author | pubmed-author:Alberto... | lld:pubmed |
| pubmed-article:11875120 | pubmed:author | pubmed-author:YesilkayaAkin... | lld:pubmed |
| pubmed-article:11875120 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11875120 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:11875120 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11875120 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11875120 | pubmed:pagination | 610-20 | lld:pubmed |
| pubmed-article:11875120 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11875120 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11875120 | pubmed:articleTitle | Independence of angiotensin II-induced MAP kinase activation from angiotensin type 1 receptor internalization in clone 9 hepatocytes. | lld:pubmed |
| pubmed-article:11875120 | pubmed:affiliation | Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510, USA. | lld:pubmed |
| pubmed-article:11875120 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11875120 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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