2022
Muscle LIM Protein Force-Sensing Mediates Sarcomeric Biomechanical Signaling in Human Familial Hypertrophic Cardiomyopathy
Riaz M, Park J, Sewanan LR, Ren Y, Schwan J, Das SK, Pomianowski PT, Huang Y, Ellis MW, Luo J, Liu J, Song L, Chen IP, Qiu C, Yazawa M, Tellides G, Hwa J, Young LH, Yang L, Marboe CC, Jacoby DL, Campbell SG, Qyang Y. Muscle LIM Protein Force-Sensing Mediates Sarcomeric Biomechanical Signaling in Human Familial Hypertrophic Cardiomyopathy. Circulation 2022, 145: 1238-1253. PMID: 35384713, PMCID: PMC9109819, DOI: 10.1161/circulationaha.121.056265.Peer-Reviewed Original ResearchConceptsHypertrophic cardiomyopathySarcomeric mutationsFamilial hypertrophic cardiomyopathySudden cardiac deathCardiac myosin heavy chainMechanism-based treatmentsDevelopment of hypertrophyActivated T cellsCalcineurin-nuclear factorForce productionPhenotypic expressionPluripotent stem cell-derived cardiomyocytesStem cell-derived cardiomyocytesHeart failureCardiac deathVentricular hypertrophyCell-derived cardiomyocytesCardiac contractilityPharmacological interventionsT cellsCardiac diseaseCardiac hypertrophyPatient-specific induced pluripotent stem cellsPharmacological meansTwitch relaxation
2021
Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation
Sewanan LR, Park J, Rynkiewicz MJ, Racca AW, Papoutsidakis N, Schwan J, Jacoby DL, Moore JR, Lehman W, Qyang Y, Campbell SG. Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation. The Journal Of General Physiology 2021, 153: e202012640. PMID: 34319370, PMCID: PMC8321830, DOI: 10.1085/jgp.202012640.Peer-Reviewed Original ResearchConceptsHypertrophic cardiomyopathyHeart tissueCellular hypertrophyEngineered Heart TissuePathological cardiac hypertrophyThin filament mutationsMavacamten treatmentDiastolic dysfunctionDisease featuresHypertrophic effectCardiac hypertrophyContractile differencesHypertrophyFundamental disease mechanismsCrossbridge activityInherited disorderOverall Ca2Uncertain significancePatient phenotypesDisease mechanismsLow Ca2PatientsK mutationMavacamtenTissue
2019
Patient mutations linked to arrhythmogenic cardiomyopathy enhance calpain-mediated desmoplakin degradation
Ng R, Manring H, Papoutsidakis N, Albertelli T, Tsai N, See CJ, Li X, Park J, Stevens TL, Bobbili PJ, Riaz M, Ren Y, Stoddard CE, Janssen PM, Bunch TJ, Hall SP, Lo YC, Jacoby DL, Qyang Y, Wright N, Ackermann MA, Campbell SG. Patient mutations linked to arrhythmogenic cardiomyopathy enhance calpain-mediated desmoplakin degradation. JCI Insight 2019, 5 PMID: 31194698, PMCID: PMC6675562, DOI: 10.1172/jci.insight.128643.Peer-Reviewed Original ResearchSarcomere-Directed Calcium Reporters in Cardiomyocytes
Campbell SG, Qyang Y, Hinson JT. Sarcomere-Directed Calcium Reporters in Cardiomyocytes. Circulation Research 2019, 124: 1151-1153. PMID: 30973804, PMCID: PMC6527368, DOI: 10.1161/circresaha.119.314877.Peer-Reviewed Original Research
2001
Bob1, a Gim5/MM-1/Pfd5 homolog, interacts with the MAP kinase kinase Byr1 to regulate sexual differentiation in the fission yeast, Schizosaccharomyces pombe
Henkel J, Du H, Yang P, Qyang Y, Kansra S, Ko M, Kim H, Marcus S. Bob1, a Gim5/MM-1/Pfd5 homolog, interacts with the MAP kinase kinase Byr1 to regulate sexual differentiation in the fission yeast, Schizosaccharomyces pombe. Differentiation 2001, 67: 98-106. PMID: 11683500, DOI: 10.1046/j.1432-0436.2001.670402.x.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceBase SequenceCatalysisCell DifferentiationConserved SequenceCytoskeletonHumansMicroscopy, FluorescenceMolecular Sequence DataMutationProtein BindingProtein KinasesRepressor ProteinsReproduction, AsexualSchizosaccharomycesSchizosaccharomyces pombe ProteinsSubstrate SpecificityThiabendazoleTwo-Hybrid System TechniquesConceptsS. pombe cellsFission yeastPombe cellsObvious growth defectTwo-hybrid screenRegulators of actinSexual differentiationInhibition of matingMating deficiencyEukaryotic organismsMAPK moduleNull mutantsS. pombeCytoskeletal controlGrowth defectCytoskeletal defectsMating responseByr1Diverse rolesMutantsMolecular characterizationYeastProteinSchizosaccharomycesOverexpressionGenetic and Molecular Characterization of Skb15, a Highly Conserved Inhibitor of the Fission Yeast PAK, Shk1
Kim H, Yang P, Qyang Y, Lai H, Du H, Henkel J, Kumar K, Bao S, Liu M, Marcus S. Genetic and Molecular Characterization of Skb15, a Highly Conserved Inhibitor of the Fission Yeast PAK, Shk1. Molecular Cell 2001, 7: 1095-1101. PMID: 11389855, DOI: 10.1016/s1097-2765(01)00248-9.Peer-Reviewed Original ResearchConceptsFission yeastP21-activated kinaseCytokinetic functionCytokinetic machineryCell polarityProtein functionSkb15Cytoskeletal remodelingMouse homologMicrotubule biogenesisShk1Mating responseNegative regulationActin polymerizationNull mutationCell cycleMolecular characterizationYeastSubstantial uncouplingProper executionPartial lossSchizosaccharomycesBiogenesisHomologKinase