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Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart
- Date Issued:
- 2003
- Summary:
- 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.
Title: | Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart. |
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Name(s): |
Jia, Yuanyuan Florida Atlantic University, Degree grantor Huang, Xupei, Thesis advisor Charles E. Schmidt College of Medicine Department of Biomedical Science |
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Type of Resource: | text | |
Genre: | Electronic Thesis Or Dissertation | |
Issuance: | monographic | |
Date Issued: | 2003 | |
Publisher: | Florida Atlantic University | |
Place of Publication: | Boca Raton, FL | |
Physical Form: | application/pdf | |
Extent: | 64 p. | |
Language(s): | English | |
Summary: | 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. | |
Identifier: | 9780496181629 (isbn), 12998 (digitool), FADT12998 (IID), fau:9865 (fedora) | |
Degree granted: | Thesis (M.S.)--Florida Atlantic University, 2003. | |
Collection: | FAU Electronic Theses and Dissertations Collection | |
Note(s): | Charles E. Schmidt College of Science | |
Subject(s): |
Mice as laboratory animals Mice--Metabolism Energy metabolism Mitochondria |
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Held by: | Florida Atlantic University Libraries | |
Persistent Link to This Record: | http://purl.flvc.org/fcla/dt/12998 | |
Sublocation: | Digital Library | |
Use and Reproduction: | Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder. | |
Use and Reproduction: | http://rightsstatements.org/vocab/InC/1.0/ | |
Host Institution: | FAU | |
Is Part of Series: | Florida Atlantic University Digital Library Collections. |