Featured Publications
Controllability analysis of the directed human protein interaction network identifies disease genes and drug targets
Vinayagam A, Gibson TE, Lee HJ, Yilmazel B, Roesel C, Hu Y, Kwon Y, Sharma A, Liu YY, Perrimon N, Barabási AL. Controllability analysis of the directed human protein interaction network identifies disease genes and drug targets. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 4976-4981. PMID: 27091990, PMCID: PMC4983807, DOI: 10.1073/pnas.1603992113.Peer-Reviewed Original ResearchConceptsPPI networkDisease genesProtein-protein interaction networkDrug targetsCellular information processingHuman PPI networkNovel disease genesCopy number alteration dataPotential drug targetsNumber alteration dataDisease-causing mutationsIndispensable proteinsInteraction networksCell deathGenesProteinCell proliferationDifferent cancersHuman virusesPrimary targetAlteration dataDisease statesTargetMutationsNetwork control properties
2020
Differential contributions of sarcomere and mitochondria-related multigene variants to the endophenotype of hypertrophic cardiomyopathy
Chung H, Kim Y, Cho SM, Lee HJ, Park CH, Kim JY, Lee SH, Min PK, Yoon YW, Lee BK, Kim WS, Hong BK, Kim TH, Rim SJ, Kwon HM, Choi EY, Lee KA. Differential contributions of sarcomere and mitochondria-related multigene variants to the endophenotype of hypertrophic cardiomyopathy. Mitochondrion 2020, 53: 48-56. PMID: 32380161, DOI: 10.1016/j.mito.2020.04.010.Peer-Reviewed Original ResearchConceptsNon-apical hypertrophic cardiomyopathyApical hypertrophic cardiomyopathyHypertrophic cardiomyopathyHCM patientsIndividualized risk stratificationComprehensive genetic testAtrium remodelingDiastolic dysfunctionRisk stratificationPoor prognosisSarcomere mutationsPatientsPathogenic variantsRare variant analysisAsian populationsPathogenic mutations
2019
NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome
Fang EF, Hou Y, Lautrup S, Jensen MB, Yang B, SenGupta T, Caponio D, Khezri R, Demarest TG, Aman Y, Figueroa D, Morevati M, Lee HJ, Kato H, Kassahun H, Lee JH, Filippelli D, Okur MN, Mangerich A, Croteau DL, Maezawa Y, Lyssiotis CA, Tao J, Yokote K, Rusten TE, Mattson MP, Jasper H, Nilsen H, Bohr VA. NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome. Nature Communications 2019, 10: 5284. PMID: 31754102, PMCID: PMC6872719, DOI: 10.1038/s41467-019-13172-8.Peer-Reviewed Original ResearchMeSH KeywordsAging, PrematureAnimalsAutophagy-Related Protein-1 HomologCaenorhabditis elegansCation Transport ProteinsDisease Models, AnimalDrosophila melanogasterHumansIntracellular Signaling Peptides and ProteinsMitophagyMutationNADNicotinamide-Nucleotide AdenylyltransferaseWerner SyndromeWerner Syndrome HelicaseConceptsWerner syndromeWerner DNA helicasePremature aging diseaseDrosophila melanogaster modelStem cell dysfunctionCaenorhabditis elegansDNA helicaseOrganismal levelImpaired mitochondrial functionMitochondrial qualityWS phenotypeImpaired mitophagyMitophagyMitochondrial functionDCT-1Ubiquitous moleculeSevere metabolic phenotypeMetabolic phenotypePhenotypeW patientsMetabolic dysfunctionCell dysfunctionMetabolic deficitsTherapeutic interventionsUnderlying mechanism