2022
Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation
Su KN, Ma Y, Cacheux M, Ilkan Z, Raad N, Muller GK, Wu X, Guerrera N, Thorn SL, Sinusas AJ, Foretz M, Viollet B, Akar JG, Akar FG, Young LH. Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation. JCI Insight 2022, 7: e141213. PMID: 35451373, PMCID: PMC9089788, DOI: 10.1172/jci.insight.141213.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsAtrial FibrillationAtrial RemodelingConnexinsIon ChannelsMiceMyocytes, CardiacTranscription FactorsConceptsTranscription factorsKey transcription factorMaster metabolic regulatorIon channel subunitsGap junction proteinTranscriptional reprogrammingAMPK deletionProtein kinaseBiological functionsTranscriptional downregulationMetabolic regulatorChannel subunitsIon channelsAMPK expressionMetabolic stressAtrial fibrillationAMPKJunction proteinsElectrical excitabilityHomeostatic roleStructural remodelingConnexinsAtrial ion channelsRemodelingDownregulation
2015
Deletion of MLIP (Muscle-enriched A-type Lamin-interacting Protein) Leads to Cardiac Hyperactivation of Akt/Mammalian Target of Rapamycin (mTOR) and Impaired Cardiac Adaptation*
Cattin ME, Wang J, Weldrick JJ, Roeske CL, Mak E, Thorn SL, DaSilva JN, Wang Y, Lusis AJ, Burgon PG. Deletion of MLIP (Muscle-enriched A-type Lamin-interacting Protein) Leads to Cardiac Hyperactivation of Akt/Mammalian Target of Rapamycin (mTOR) and Impaired Cardiac Adaptation*. Journal Of Biological Chemistry 2015, 290: 26699-26714. PMID: 26359501, PMCID: PMC4646324, DOI: 10.1074/jbc.m115.678433.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsCardiomegalyCarrier ProteinsCo-Repressor ProteinsFemaleGene Expression RegulationGenome-Wide Association StudyHeart Function TestsHemodynamicsIsoproterenolMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacNuclear ProteinsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionStress, PhysiologicalTOR Serine-Threonine KinasesUltrasonographyConceptsAKT/mTOR pathwayGenome-wide association studiesAkt/mammalian targetMTOR pathwayAkt/mTOR activityAkt/mTORUnique proteinsUnknown functionAssociation studiesMTOR activityMammalian targetCardiac adaptationRegenerative abilityGenetic associationAdult heartPathwayHomeostasisMyocardial metabolic abnormalitiesNormal cardiac functionAdaptationEarly responseMetabolic abnormalitiesCardiac functionMLIPCardiac stress
2009
Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen
Folmes KD, Chan AY, Koonen DP, Pulinilkunnil TC, Baczkó I, Hunter BE, Thorn S, Allard MF, Roberts R, Gollob MH, Light PE, Dyck JR. Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen. Circulation Genomic And Precision Medicine 2009, 2: 457-466. PMID: 20031621, DOI: 10.1161/circgenetics.108.834564.Peer-Reviewed Original ResearchConceptsTransgenic miceR302Q mutationGlycogen contentAcute expressionCardiomyocyte-restricted expressionAMPK activationTransgenic adult miceNeonatal rat cardiomyocytesChronic modelWolff-ParkinsonGlycogen synthase activityWhite syndromeCardiac hypertrophyAdult miceGlycogen storage cardiomyopathyMyocardial glycogenDirect effectCompensatory alterationsRat cardiomyocytesFamilial formsMiceEarly signaling eventCardiomyopathyAMPK activityHeart