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Identification of a truncated form of methionine sulfoxide reductase a expressed in mouse embryonic stem cells
Title
Identification of a truncated form of methionine sulfoxide reductase a expressed in mouse embryonic stem cells.
Creator
Jia, Pingping, Zhang, Chi, Jia, Yuanyuan, Webster, Keith A., Huang, Xupei, Kochegarov, Andrei A., Lemanski, Sharon L., Lemanski, Larry F.
Date Issued
2011-06-22
PURL
http://purl.flvc.org/fcla/dt/3327268
Subject Headings
Cell nucleus -- metabolism, Cloning, Molecular, Cytosol --metabolism, Embryonic Stem Cells --metabolism, Methionine --metabolism, Methionine Sulfoxide Reductases, Methionine Sulfoxide Reductases --metabolism, Methionine Sulfoxide Reductases --genetics, Mitochondria --metabolism, Molecular Sequence Data, Oxidation --Reduction, Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Methionine
Format
Document (PDF)
Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart
Title
Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart.
Creator
Jia, Yuanyuan, Florida Atlantic University, Huang, Xupei, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description
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...
Show moreTroponin 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.
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Date Issued
2003
PURL
http://purl.flvc.org/fcla/dt/12998
Subject Headings
Mice as laboratory animals, Mice--Metabolism, Energy metabolism, Mitochondria
Format
Document (PDF)