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dc.contributor.authorZhang, Pingbo
dc.contributor.authorMurphy, Anne M.
dc.contributor.authorKass, David A.
dc.contributor.authorRamirez-Correa, Genaro
dc.contributor.authorKeceli, Gizem
dc.contributor.authorHeravi, Amir
dc.contributor.authorOkumus, Nazli
dc.contributor.authorTakahashi, Cyrus
dc.contributor.authorLi, Yuejin
dc.contributor.authorZhu, Guangshuo
dc.contributor.authorPaolocci, Nazareno
dc.date.accessioned2021-03-03T15:24:05Z
dc.date.available2021-03-03T15:24:05Z
dc.date.issued2017
dc.identifier.citationLi Y., Zhu G., Paolocci N., Zhang P., Takahashi C., Okumus N., Heravi A., Keceli G., Ramirez-Correa G., Kass D. A. , et al., "Heart Failure-Related Hyperphosphorylation in the Cardiac Troponin I C Terminus Has Divergent Effects on Cardiac Function In Vivo", CIRCULATION-HEART FAILURE, cilt.10, sa.9, 2017
dc.identifier.issn1941-3289
dc.identifier.othervv_1032021
dc.identifier.otherav_3ecdb6a5-620e-4eb5-99b6-f5d2d56c3b03
dc.identifier.urihttp://hdl.handle.net/20.500.12627/46056
dc.identifier.urihttps://doi.org/10.1161/circheartfailure.117.003850
dc.description.abstractBACKGROUND: In human heart failure, Ser199 (equivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated, and in vitro studies suggest that it enhances myofilament calcium sensitivity and alters calpain-mediated cTnI proteolysis. However, how its hyperphosphorylation affects cardiac function in vivo remains unknown.
dc.language.isoeng
dc.subjectCARDIAC ve CARDIOVASCULAR SİSTEMLER
dc.subjectKlinik Tıp
dc.subjectKlinik Tıp (MED)
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectKardiyoloji
dc.titleHeart Failure-Related Hyperphosphorylation in the Cardiac Troponin I C Terminus Has Divergent Effects on Cardiac Function In Vivo
dc.typeMakale
dc.relation.journalCIRCULATION-HEART FAILURE
dc.contributor.departmentJohns Hopkins University , ,
dc.identifier.volume10
dc.identifier.issue9
dc.contributor.firstauthorID245381


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