pubmed-article:19685039 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C0151744 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C0034826 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C0257694 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:19685039 | lifeskim:mentions | umls-concept:C1882911 | lld:lifeskim |
pubmed-article:19685039 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:19685039 | pubmed:dateCreated | 2009-10-21 | lld:pubmed |
pubmed-article:19685039 | pubmed:abstractText | We have studied the association between M(3) muscarinic acetylcholine receptors (M(3)-mAChR) and protein kinase C-epsilon (PKC-epsilon) during ischemic myocardial injury using Western blot analysis and immunoprecipitation technique. Myocardial ischemia (MI) induced PKC-epsilon translocation from cytosolic to membrane fractions. This translocation participated in the phosphorylation of M(3)-mAChR in membrane fractions, which could be abolished by the inhibitor of PKC, chelerythrine chloride. On the other hand, M(3)-mAChR could also regulate the expression of PKC-epsilon in ischemic myocardium. Choline (choline chloride, an M(3) receptor agonist, administered at 15 min before occlusion) strengthened the association between PKC-epsilon and M(3)-mAChR. However, blockade of M(3)-mAChR by 4-diphenylacetoxy-N-methylpiperidine methiodide (an M(3) receptor antagonist, administered at 20 min before occlusion) completely inhibited the effect of choline on the expression of PKC-epsilon. We conclude that the translocation of PKC-epsilon is required for the phosphorylation of M(3)-mAChR; moreover, increased PKC-epsilon activity is associated with M(3)-mAChR during MI. This reciprocal regulation is likely to play a role in heart signal transduction during ischemia between ventricular myocytes. | lld:pubmed |
pubmed-article:19685039 | pubmed:language | eng | lld:pubmed |
pubmed-article:19685039 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19685039 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19685039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19685039 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19685039 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19685039 | pubmed:month | Nov | lld:pubmed |
pubmed-article:19685039 | pubmed:issn | 1432-1912 | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:ZhangYongY | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:ZhaoJingJ | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:ZhaoNaN | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:YangLi-liLL | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:SunLi-huaLH | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:WangYu-pingYP | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:DuZhi-minZM | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:HangPeng-zhou... | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:SunZhi-danZD | lld:pubmed |
pubmed-article:19685039 | pubmed:author | pubmed-author:MaoYu-yingYY | lld:pubmed |
pubmed-article:19685039 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19685039 | pubmed:volume | 380 | lld:pubmed |
pubmed-article:19685039 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19685039 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19685039 | pubmed:pagination | 443-50 | lld:pubmed |
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pubmed-article:19685039 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19685039 | pubmed:articleTitle | Reciprocal regulation between M3 muscarinic acetylcholine receptor and protein kinase C-epsilon in ventricular myocytes during myocardial ischemia in rats. | lld:pubmed |
pubmed-article:19685039 | pubmed:affiliation | Institute of Clinical Pharmacology of Second Hospital, Harbin Medical University, Key Laboratory of Heilongjiang Province, Baojian Road 157, Nangang District, Harbin, Heilongjiang Province, 150081, People's Republic of China. | lld:pubmed |
pubmed-article:19685039 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19685039 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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