Linked Life Data

14499869

Source:http://linkedlifedata.com/resource/pubmed/id/14499869

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pubmed-article:14499869pubmed:abstractTextPossession of the C34T (Glu12Stop) nonsense mutation in the AMP-deaminase 1 (AMPD1) gene has been shown to be associated with improved prognosis in heart failure and ischemic heart disease. The most likely event leading to these clinical effects is a reduced capacity of the AMP deamination pathway and increased production of cardio-protective adenosine. However, since AMPD1 is predominantly expressed in skeletal muscle, the protective effects could be related not only to local cardiac changes, but also to a systemic mechanism. In the present study we evaluated the effect of the C34T mutation on cardiac AMP-deaminase activity and on the systemic changes in adenosine production.lld:pubmed
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pubmed-article:14499869pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:14499869pubmed:articleTitleDecreased cardiac activity of AMP deaminase in subjects with the AMPD1 mutation--a potential mechanism of protection in heart failure.lld:pubmed
pubmed-article:14499869pubmed:affiliationHeart Science Centre, Imperial College at Harefield Hospital, Harefield, Middlesex UB9 6JH, UK.lld:pubmed
pubmed-article:14499869pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:14499869pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:14499869pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed