pubmed-article:19289642 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19289642 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
pubmed-article:19289642 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:19289642 | lifeskim:mentions | umls-concept:C0694883 | lld:lifeskim |
pubmed-article:19289642 | lifeskim:mentions | umls-concept:C0073096 | lld:lifeskim |
pubmed-article:19289642 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:19289642 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:19289642 | pubmed:dateCreated | 2009-3-31 | lld:pubmed |
pubmed-article:19289642 | pubmed:abstractText | Master regulators of protein synthesis such as mammalian target of rapamycin (mTOR) and p70S6 kinase contribute to left ventricular hypertrophy. These prohypertrophic pathways are modulated by a number of kinase cascades, including the hierarchical LKB1/AMP-activated protein kinase (AMPK) energy-sensing pathway. Because oxidative stress inhibits the LKB1/AMPK signaling axis to promote abnormal cell growth in cancer cells, we investigated whether oxidative stress associated with hypertension also results in the inhibition of this kinase circuit to contribute to left ventricular hypertrophy. | lld:pubmed |
pubmed-article:19289642 | pubmed:language | eng | lld:pubmed |
pubmed-article:19289642 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19289642 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:19289642 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19289642 | pubmed:month | Mar | lld:pubmed |
pubmed-article:19289642 | pubmed:issn | 1524-4539 | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:DyckJason R... | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:LightPeter... | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:DolinskyVerno... | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:Des... | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:ChanAnita Y... | lld:pubmed |
pubmed-article:19289642 | pubmed:author | pubmed-author:Robillard... | lld:pubmed |
pubmed-article:19289642 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19289642 | pubmed:day | 31 | lld:pubmed |
pubmed-article:19289642 | pubmed:volume | 119 | lld:pubmed |
pubmed-article:19289642 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19289642 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19289642 | pubmed:pagination | 1643-52 | lld:pubmed |
pubmed-article:19289642 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:19289642 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19289642 | pubmed:articleTitle | Resveratrol prevents the prohypertrophic effects of oxidative stress on LKB1. | lld:pubmed |
pubmed-article:19289642 | pubmed:affiliation | Cardiovascular Research Group, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta T6G2S2, Canada. | lld:pubmed |
pubmed-article:19289642 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19289642 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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