Partial replacement of cardiac troponin I with a non-phosphorylatable mutant at serines 43/45 attenuates the contractile dysfunction associated with PKCepsilon phosphorylation.
Scruggs, Sarah B
Partial replacement of cardiac troponin I with a non-phosphorylatable mutant at serines 43/45 attenuates the contractile dysfunction associated with PKCepsilon phosphorylation. [electronic resource] - Journal of molecular and cellular cardiology Apr 2006 - 465-73 p. digital
Publication Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
0022-2828
10.1016/j.yjmcc.2005.12.009 doi
Aging--genetics
Amino Acid Substitution
Animals
Cell Line
Heart Failure--genetics
Mice
Mice, Transgenic
Myocardial Contraction--genetics
Myocardium--metabolism
Phosphorylation
Protein Kinase C-epsilon--metabolism
Protein Processing, Post-Translational--genetics
Troponin I--genetics
Ventricular Function, Left--genetics
Partial replacement of cardiac troponin I with a non-phosphorylatable mutant at serines 43/45 attenuates the contractile dysfunction associated with PKCepsilon phosphorylation. [electronic resource] - Journal of molecular and cellular cardiology Apr 2006 - 465-73 p. digital
Publication Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
0022-2828
10.1016/j.yjmcc.2005.12.009 doi
Aging--genetics
Amino Acid Substitution
Animals
Cell Line
Heart Failure--genetics
Mice
Mice, Transgenic
Myocardial Contraction--genetics
Myocardium--metabolism
Phosphorylation
Protein Kinase C-epsilon--metabolism
Protein Processing, Post-Translational--genetics
Troponin I--genetics
Ventricular Function, Left--genetics