Distinct early signaling events resulting from the expression of the PRKAG2 R302Q mutant of AMPK contribute to increased myocardial glycogen.
Identifieur interne : 002011 ( Main/Merge ); précédent : 002010; suivant : 002012Distinct early signaling events resulting from the expression of the PRKAG2 R302Q mutant of AMPK contribute to increased myocardial glycogen.
Auteurs : Karalyn D. Folmes [Canada] ; Anita Y M. Chan ; Debby P Y. Koonen ; Thomas C. Pulinilkunnil ; István Baczk ; Beth E. Hunter ; Stephanie Thorn ; Michael F. Allard ; Robert Roberts ; Michael H. Gollob ; Peter E. Light ; Jason R B. DyckSource :
- Circulation. Cardiovascular genetics [ 1942-3268 ] ; 2009.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (genetics), AMP-Activated Protein Kinases (metabolism), Animals, Cells, Cultured, Disease Models, Animal, Female, Gene Expression, Glycogen (metabolism), Humans, Male, Mice, Mice, Transgenic, Mutation, Missense, Myocytes, Cardiac (metabolism), Rats, Signal Transduction, Wolff-Parkinson-White Syndrome (enzymology), Wolff-Parkinson-White Syndrome (genetics).
- MESH :
- chemical , genetics : AMP-Activated Protein Kinases.
- chemical , metabolism : AMP-Activated Protein Kinases, Glycogen.
- enzymology : Wolff-Parkinson-White Syndrome.
- genetics : Wolff-Parkinson-White Syndrome.
- metabolism : Myocytes, Cardiac.
- Animals, Cells, Cultured, Disease Models, Animal, Female, Gene Expression, Humans, Male, Mice, Mice, Transgenic, Mutation, Missense, Rats, Signal Transduction.
Abstract
Humans with an R302Q mutation in AMPKgamma(2) (the PRKAG2 gene) develop a glycogen storage cardiomyopathy characterized by a familial form of Wolff-Parkinson-White syndrome and cardiac hypertrophy. This phenotype is recapitulated in transgenic mice with cardiomyocyte-restricted expression of AMPKgamma(2)R302Q. Although considerable information is known regarding the consequences of harboring the gamma(2)R302Q mutation, little is known about the early signaling events that contribute to the development of this cardiomyopathy.
DOI: 10.1161/CIRCGENETICS.108.834564
PubMed: 20031621
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pubmed:20031621Le document en format XML
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Chan</name></author><author><name sortKey="Koonen, Debby P Y" sort="Koonen, Debby P Y" uniqKey="Koonen D" first="Debby P Y" last="Koonen">Debby P Y. Koonen</name></author><author><name sortKey="Pulinilkunnil, Thomas C" sort="Pulinilkunnil, Thomas C" uniqKey="Pulinilkunnil T" first="Thomas C" last="Pulinilkunnil">Thomas C. Pulinilkunnil</name></author><author><name sortKey="Baczk, Istvan" sort="Baczk, Istvan" uniqKey="Baczk I" first="István" last="Baczk">István Baczk</name></author><author><name sortKey="Hunter, Beth E" sort="Hunter, Beth E" uniqKey="Hunter B" first="Beth E" last="Hunter">Beth E. Hunter</name></author><author><name sortKey="Thorn, Stephanie" sort="Thorn, Stephanie" uniqKey="Thorn S" first="Stephanie" last="Thorn">Stephanie Thorn</name></author><author><name sortKey="Allard, Michael F" sort="Allard, Michael F" uniqKey="Allard M" first="Michael F" last="Allard">Michael F. Allard</name></author><author><name sortKey="Roberts, Robert" sort="Roberts, Robert" uniqKey="Roberts R" first="Robert" last="Roberts">Robert Roberts</name></author><author><name sortKey="Gollob, Michael H" sort="Gollob, Michael H" uniqKey="Gollob M" first="Michael H" last="Gollob">Michael H. Gollob</name></author><author><name sortKey="Light, Peter E" sort="Light, Peter E" uniqKey="Light P" first="Peter E" last="Light">Peter E. Light</name></author><author><name sortKey="Dyck, Jason R B" sort="Dyck, Jason R B" uniqKey="Dyck J" first="Jason R B" last="Dyck">Jason R B. 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Folmes</name><affiliation wicri:level="1"><nlm:affiliation>Cardiovascular Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Cardiovascular Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta</wicri:regionArea><wicri:noRegion>Alberta</wicri:noRegion></affiliation></author><author><name sortKey="Chan, Anita Y M" sort="Chan, Anita Y M" uniqKey="Chan A" first="Anita Y M" last="Chan">Anita Y M. Chan</name></author><author><name sortKey="Koonen, Debby P Y" sort="Koonen, Debby P Y" uniqKey="Koonen D" first="Debby P Y" last="Koonen">Debby P Y. Koonen</name></author><author><name sortKey="Pulinilkunnil, Thomas C" sort="Pulinilkunnil, Thomas C" uniqKey="Pulinilkunnil T" first="Thomas C" last="Pulinilkunnil">Thomas C. Pulinilkunnil</name></author><author><name sortKey="Baczk, Istvan" sort="Baczk, Istvan" uniqKey="Baczk I" first="István" last="Baczk">István Baczk</name></author><author><name sortKey="Hunter, Beth E" sort="Hunter, Beth E" uniqKey="Hunter B" first="Beth E" last="Hunter">Beth E. Hunter</name></author><author><name sortKey="Thorn, Stephanie" sort="Thorn, Stephanie" uniqKey="Thorn S" first="Stephanie" last="Thorn">Stephanie Thorn</name></author><author><name sortKey="Allard, Michael F" sort="Allard, Michael F" uniqKey="Allard M" first="Michael F" last="Allard">Michael F. Allard</name></author><author><name sortKey="Roberts, Robert" sort="Roberts, Robert" uniqKey="Roberts R" first="Robert" last="Roberts">Robert Roberts</name></author><author><name sortKey="Gollob, Michael H" sort="Gollob, Michael H" uniqKey="Gollob M" first="Michael H" last="Gollob">Michael H. Gollob</name></author><author><name sortKey="Light, Peter E" sort="Light, Peter E" uniqKey="Light P" first="Peter E" last="Light">Peter E. Light</name></author><author><name sortKey="Dyck, Jason R B" sort="Dyck, Jason R B" uniqKey="Dyck J" first="Jason R B" last="Dyck">Jason R B. Dyck</name></author></analytic><series><title level="j">Circulation. Cardiovascular genetics</title><idno type="eISSN">1942-3268</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (genetics)</term><term>AMP-Activated Protein Kinases (metabolism)</term><term>Animals</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Glycogen (metabolism)</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation, Missense</term><term>Myocytes, Cardiac (metabolism)</term><term>Rats</term><term>Signal Transduction</term><term>Wolff-Parkinson-White Syndrome (enzymology)</term><term>Wolff-Parkinson-White Syndrome (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>AMP-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term><term>Glycogen</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Wolff-Parkinson-White Syndrome</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Wolff-Parkinson-White Syndrome</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation, Missense</term><term>Rats</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Humans with an R302Q mutation in AMPKgamma(2) (the PRKAG2 gene) develop a glycogen storage cardiomyopathy characterized by a familial form of Wolff-Parkinson-White syndrome and cardiac hypertrophy. This phenotype is recapitulated in transgenic mice with cardiomyocyte-restricted expression of AMPKgamma(2)R302Q. Although considerable information is known regarding the consequences of harboring the gamma(2)R302Q mutation, little is known about the early signaling events that contribute to the development of this cardiomyopathy.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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