scholarly journals Calcium desensitization in cardiac troponin C: a novel role in mouse skeletal muscle

2019 ◽  
Vol 597 (5) ◽  
pp. 1227-1229
Author(s):  
Matthew J. Novello ◽  
MengQi Zhang ◽  
Hannah E. Snyder ◽  
Qi‐Tong Lin
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin C ◽  
Mouse Skeletal Muscle ◽  
Cardiac Troponin C ◽  
Calcium Desensitization

scholarly journals Calcium-independent activation of skeletal muscle fibers by a modified form of cardiac troponin C

1993 ◽  
Vol 64 (5) ◽  
pp. 1632-1637 ◽  
Author(s):  
J.D. Hannon ◽  
P.B. Chase ◽  
D.A. Martyn ◽  
L.L. Huntsman ◽  
M.J. Kushmerick ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Muscle Fibers ◽  
Troponin C ◽  
Cardiac Troponin C ◽  
Skeletal Muscle Fibers

Identification and characterization of a cardiac-specific transcriptional regulatory element in the slow/cardiac troponin C gene

1992 ◽  
Vol 12 (5) ◽  
pp. 1967-1976
Author(s):  
M S Parmacek ◽  
A J Vora ◽  
T Shen ◽  
E Barr ◽  
F Jung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Protein Binding ◽  
Cardiac Myocytes ◽  
Cardiac Troponin ◽  
Nuclear Protein ◽  
Troponin C ◽  
Cardiac Troponin C ◽  
Transcriptional Regulatory ◽  
Skeletal Myotubes

The slow/cardiac troponin C (cTnC) gene has been used as a model system for defining the molecular mechanisms that regulate cardiac and skeletal muscle-specific gene expression during mammalian development. cTnC is expressed continuously in both embryonic and adult cardiac myocytes but is expressed only transiently in embryonic fast skeletal myotubes. We have reported previously that cTnC gene expression in skeletal myotubes is controlled by a developmentally regulated, skeletal muscle-specific transcriptional enhancer located within the first intron of the gene (bp 997 to 1141). In this report, we show that cTnC gene expression in cardiac myocytes both in vitro and in vivo is regulated by a distinct and independent transcriptional promoter and enhancer located within the immediate 5' flanking region of the gene (bp -124 to +32). DNase I footprint and electrophoretic mobility shift assay analyses demonstrated that this cardiac-specific promoter/enhancer contains five nuclear protein binding sites (designated CEF1, CEF-2, and CPF1-3), four of which bind novel cardiac-specific nuclear protein complexes. Functional analysis of the cardiac-specific cTnC enhancer revealed that mutation of either the CEF-1 or CEF-2 nuclear protein binding site abolished the activity of the cTnC enhancer in cardiac myocytes. Taken together, these results define a novel mechanism for developmentally regulating a single gene in multiple muscle cell lineages. In addition, they identify previously undefined cardiac-specific transcriptional regulatory motifs and trans-acting factors. Finally, they demonstrate distinct transcriptional regulatory pathways in cardiac and skeletal muscle.

scholarly journals Identification and characterization of a cardiac-specific transcriptional regulatory element in the slow/cardiac troponin C gene.

1992 ◽  
Vol 12 (5) ◽  
pp. 1967-1976 ◽  
Author(s):  
M S Parmacek ◽  
A J Vora ◽  
T Shen ◽  
E Barr ◽  
F Jung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Protein Binding ◽  
Cardiac Myocytes ◽  
Cardiac Troponin ◽  
Nuclear Protein ◽  
Troponin C ◽  
Cardiac Troponin C ◽  
Transcriptional Regulatory ◽  
Skeletal Myotubes

The slow/cardiac troponin C (cTnC) gene has been used as a model system for defining the molecular mechanisms that regulate cardiac and skeletal muscle-specific gene expression during mammalian development. cTnC is expressed continuously in both embryonic and adult cardiac myocytes but is expressed only transiently in embryonic fast skeletal myotubes. We have reported previously that cTnC gene expression in skeletal myotubes is controlled by a developmentally regulated, skeletal muscle-specific transcriptional enhancer located within the first intron of the gene (bp 997 to 1141). In this report, we show that cTnC gene expression in cardiac myocytes both in vitro and in vivo is regulated by a distinct and independent transcriptional promoter and enhancer located within the immediate 5' flanking region of the gene (bp -124 to +32). DNase I footprint and electrophoretic mobility shift assay analyses demonstrated that this cardiac-specific promoter/enhancer contains five nuclear protein binding sites (designated CEF1, CEF-2, and CPF1-3), four of which bind novel cardiac-specific nuclear protein complexes. Functional analysis of the cardiac-specific cTnC enhancer revealed that mutation of either the CEF-1 or CEF-2 nuclear protein binding site abolished the activity of the cTnC enhancer in cardiac myocytes. Taken together, these results define a novel mechanism for developmentally regulating a single gene in multiple muscle cell lineages. In addition, they identify previously undefined cardiac-specific transcriptional regulatory motifs and trans-acting factors. Finally, they demonstrate distinct transcriptional regulatory pathways in cardiac and skeletal muscle.

scholarly journals Mutation of the high affinity calcium binding sites in cardiac troponin C.

1992 ◽  
Vol 267 (2) ◽  
pp. 825-831 ◽  
Author(s):  
J C Negele ◽  
D G Dotson ◽  
W Liu ◽  
H L Sweeney ◽  
J A Putkey
Keyword(s):  
Binding Sites ◽  
Calcium Binding ◽  
Cardiac Troponin ◽  
Troponin C ◽  
High Affinity ◽  
Cardiac Troponin C ◽  
Calcium Binding Sites
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