Leonid Tyan, PhD
Associate Research ScientistCards
About
Research
Publications
2025
TMBIM4 affects left-right patterning via pluripotency exit during gastrulation
Diab N, Kostiuk V, Tyan L, Mis E, Zenisek D, Khokha M. TMBIM4 affects left-right patterning via pluripotency exit during gastrulation. Developmental Biology 2025, 527: 136-146. PMID: 40744297, DOI: 10.1016/j.ydbio.2025.07.018.Peer-Reviewed Original ResearchConceptsCongenital heart diseaseCongenital heart disease patientsCongenital heart disease genesIon channelsPluripotency exitPluripotency marker expressionDeleterious genetic variationLR patterningCell fate determinationApplication of cholinePutative ion channelsCardiac asymmetryCongenital defectsMarker expressionEvolutionary conservationHeart diseaseGenomic studiesProtein 4Xenopus tropicalisGastrulation defectsFate determinationGenetic variationAsymmetry defectsTMBIM4Plasma membrane
2023
Author Correction: Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR
Sempou E, Kostiuk V, Zhu J, Cecilia Guerra M, Tyan L, Hwang W, Camacho-Aguilar E, Caplan M, Zenisek D, Warmflash A, Owens N, Khokha M. Author Correction: Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR. Nature Communications 2023, 14: 3264. PMID: 37277326, PMCID: PMC10241910, DOI: 10.1038/s41467-023-39025-z.Peer-Reviewed Original Research
2022
Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR
Sempou E, Kostiuk V, Zhu J, Cecilia Guerra M, Tyan L, Hwang W, Camacho-Aguilar E, Caplan M, Zenisek D, Warmflash A, Owens N, Khokha M. Membrane potential drives the exit from pluripotency and cell fate commitment via calcium and mTOR. Nature Communications 2022, 13: 6681. PMID: 36335122, PMCID: PMC9637099, DOI: 10.1038/s41467-022-34363-w.Peer-Reviewed Original ResearchConceptsPluripotent cellsAdult tissue homeostasisCell fate commitmentDifferentiated cell fatesLeft-right patterningPluripotent embryonic cellsHuman embryonic stem cellsTemporal transcriptome analysisGene regulatory networksExpense of differentiationEmbryonic stem cellsGerm layer differentiationMembrane depolarizationFate commitmentPluripotent stateCell fateTranscriptome analysisRegulatory networksMyogenic lineageEmbryonic developmentTissue homeostasisDifferentiated fateEmbryonic cellsCandidate genesPluripotencyCaveolin-3 prevents swelling-induced membrane damage via regulation of I Cl,swell activity
Turner D, Tyan L, DeGuire F, Medvedev R, Stroebel S, Lang D, Glukhov A. Caveolin-3 prevents swelling-induced membrane damage via regulation of I Cl,swell activity. Biophysical Journal 2022, 121: 1643-1659. PMID: 35378081, PMCID: PMC9117929, DOI: 10.1016/j.bpj.2022.04.001.Peer-Reviewed Original Research
2021
Caveolin-3 is required for regulation of transient outward potassium current by angiotensin II in mouse atrial myocytes
Tyan L, Turner D, Komp K, Medvedev R, Lim E, Glukhov A. Caveolin-3 is required for regulation of transient outward potassium current by angiotensin II in mouse atrial myocytes. AJP Heart And Circulatory Physiology 2021, 320: h787-h797. PMID: 33416459, PMCID: PMC8082791, DOI: 10.1152/ajpheart.00569.2020.Peer-Reviewed Original ResearchConceptsMouse atrial myocytesTransient outward potassium currentAtrial myocytesAngiotensin IICaveolin-3Potassium currentProtein kinase CReceptor 1Cardiac ion currentsAngiotensin II receptor 1Regulation of cardiac electrophysiologyInhibition of protein kinase CEffects of AngIIRenin-angiotensin systemProtein caveolin-3Associated with caveolaeWT miceAngII receptorsAtrial remodelingMyocytesAngIIAngiotensinProtein expressionMiceCaveolae structure
2020
A compartmentalized mathematical model of mouse atrial myocytes
Asfaw T, Tyan L, Glukhov A, Bondarenko V. A compartmentalized mathematical model of mouse atrial myocytes. AJP Heart And Circulatory Physiology 2020, 318: h485-h507. PMID: 31951471, PMCID: PMC7099449, DOI: 10.1152/ajpheart.00460.2019.Peer-Reviewed Original ResearchConceptsMouse atrial myocytesIntracellular Ca2+ .Right atrial myocytesAtrial myocytesAction potentialsSmall-conductanceTransverse-axial tubule systemAction potential repolarizationAction potential generationExperimental mouse modelCardiac rhythm disordersIonic mechanismsMouse atriaSimulated action potentialsMechanisms of action potential generationVentricular myocytesT-typeAtrial fibrillationAtrial physiologyMyocytesMouse modelRhythm disordersLocal controlMiceTubule system
2019
Atrial fibrillation risk loci interact to modulate Ca2+-dependent atrial rhythm homeostasis
Laforest B, Dai W, Tyan L, Lazarevic S, Shen K, Gadek M, Broman M, Weber C, Moskowitz I. Atrial fibrillation risk loci interact to modulate Ca2+-dependent atrial rhythm homeostasis. Journal Of Clinical Investigation 2019, 129: 4937-4950. PMID: 31609246, PMCID: PMC6819107, DOI: 10.1172/jci124231.Peer-Reviewed Original ResearchConceptsAtrial rhythm controlCalcium fluxTbx5 haploinsufficiencyRhythm controlAtrial fibrillationProlonged action potential durationCa2+-ATPase inhibitorRisk lociAction potential durationPrevalent cardiac arrhythmiaGenetic risk lociGenetic association dataArrhythmia susceptibilityPotential durationRhythm instabilityAF susceptibilityNKX2-5AF propensityGata4 haploinsufficiencyCardiac developmentAF pathophysiologyAF riskCardiac arrhythmiasCardiac rhythmHaploinsufficiencyCaveolae‐Mediated Activation of Mechanosensitive Chloride Channels in Pulmonary Veins Triggers Atrial Arrhythmogenesis
Egorov Y, Lang D, Tyan L, Turner D, Lim E, Piro Z, Hernandez J, Lodin R, Wang R, Schmuck E, Raval A, Ralphe C, Kamp T, Rosenshtraukh L, Glukhov A. Caveolae‐Mediated Activation of Mechanosensitive Chloride Channels in Pulmonary Veins Triggers Atrial Arrhythmogenesis. Journal Of The American Heart Association 2019, 8: e012748. PMID: 31597508, PMCID: PMC6818041, DOI: 10.1161/jaha.119.012748.Peer-Reviewed Original ResearchConceptsAtrial fibrillationPulmonary veinsAtrial dilatationRat PVChloride channelsDecreased action potential amplitudeDevelopment of atrial fibrillationParoxysmal atrial fibrillationEctopic beatsAction potential amplitudePatch-clamp studiesChronically elevated blood pressureDisruption of caveolae structureElevated blood pressureChloride channel 3Spontaneously Hypertensive RatsChloride ion channelStretch-induced activationCardiomyocyte stretchChronic hypertensionAtrial arrhythmogenesisClC-3Atrial arrhythmiasPolymerase chain reactionMembrane depolarizationA calcium transport mechanism for atrial fibrillation in Tbx5-mutant mice
Dai W, Laforest B, Tyan L, Shen K, Nadadur R, Alvarado F, Mazurek S, Lazarevic S, Gadek M, Wang Y, Li Y, Valdivia H, Shen L, Broman M, Moskowitz I, Weber C. A calcium transport mechanism for atrial fibrillation in Tbx5-mutant mice. ELife 2019, 8: e41814. PMID: 30896405, PMCID: PMC6428569, DOI: 10.7554/elife.41814.Peer-Reviewed Original ResearchConceptsTrans-sarcolemmal calcium fluxAtrial fibrillationSarcoplasmic reticulumCalcium fluxAction potentialsAF riskSR calcium uptakeCellular Ca2+ homeostasisCalcium transport mechanismsT-box transcription factor Tbx5Cardiomyocyte action potentialSERCA functionSERCA2 activityAtrial cardiomyocytesSpontaneous AFTranscription factor Tbx5Tbx5 deficiencyHuman arrhythmiasCalcium uptakeTriggered activityTranscriptional controlGenetic implicationsTbx5CardiomyocytesT-boxDisruption of Caveolar Microdomains Creates “Hot Spots” for Atrial Ectopy and Arrythmogenesis in Heart Failure Mice
Lang D, Tyan L, Warden A, Piro Z, Lodin R, Lim E, Irwin A, Glukhov A. Disruption of Caveolar Microdomains Creates “Hot Spots” for Atrial Ectopy and Arrythmogenesis in Heart Failure Mice. Biophysical Journal 2019, 116: 232a. DOI: 10.1016/j.bpj.2018.11.1273.Peer-Reviewed Original Research
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