Date of Award
2003
Document Type
Thesis
Publication Status
Version of Record
Submission Date
October 2026
Thesis/Dissertation Advisor [Chair]
Huang, Xupei
Abstract
Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
Extent
64 p.
Recommended Citation
Jia, Yuanyuan, "Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart" (2003). Electronic Theses and Dissertations 2000 - 2009. 539.
https://digitalcommons.fau.edu/etd_general_5/539
Identifier
FADT12998
Comments
Charles E. Schmidt College of Science|Thesis (M.S.)--Florida Atlantic University, 2003.|FAU Electronic Theses and Dissertations Collection|Charles E. Schmidt College of Science