Phosphorylation or Glutamic Acid Substitution at Protein Kinase C Sites on Cardiac Troponin I Differentially Depress Myofilament Tension and Shortening Velocity-Reference-Cited by-同舟云学术

Phosphorylation or Glutamic Acid Substitution at Protein Kinase C Sites on Cardiac Troponin I Differentially Depress Myofilament Tension and Shortening Velocity

Published:2003-03 Issue:13 Volume:278 Page:11265-11272
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Burkart Eileen M.,Sumandea Marius P.,Kobayashi Tomoyoshi,Nili Mahta,Martin Anne F.,Homsher Earl,Solaro R. John

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference49 articles.

1. Ca2+ activation of myofilaments from transgenic mouse hearts expressing R92Q mutant cardiac troponin T

2. Inotropic Stimulation Induces Cardiac Dysfunction in Transgenic Mice Expressing a Troponin T (I79N) Mutation Linked to Familial Hypertrophic Cardiomyopathy

3. Integration of Cardiac Myofilament Activity and Regulation with Pathways Signaling Hypertrophy and Failure

4. Functional Defects in Troponin and the Systems Biology of Heart Failure

5. Effects of Protein Kinase A Phosphorylation on Signaling between Cardiac Troponin I and the N-Terminal Domain of Cardiac Troponin C

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