TNNI3K is a novel mediator of myofilament function and phosphorylates cardiac troponin I

Author:

Wang Hui,Wang Lin,Song Li1,Zhang Yan-Wan1,Ye Jue1,Xu Rui-Xia1,Shi Na1,Meng Xian-Min1

Affiliation:

1. Chinese Academy of Medical Sciences and Peking Union Medical College, China

Publisher

FapUNIFESP (SciELO)

Subject

Cell Biology,General Pharmacology, Toxicology and Pharmaceutics,General Medicine,Immunology,Physiology,Biochemistry,General Neuroscience,Biophysics

Reference35 articles.

1. Cloning and characterization of a novel cardiac-specific kinase that interacts specifically with cardiac troponin I;Zhao Y;J Mol Med,2003

2. The protein kinase complement of the human genome;Manning G;Science,2002

3. Identification of the dual specificity and the functional domains of the cardiac-specific protein kinase TNNI3K;Feng Y;Gen Physiol Biophys,2007

4. AOP-1 interacts with cardiac-specific protein kinase TNNI3K and down-regulates its kinase activity;Feng Y;Biochemistry,2007

5. Structural consequences of cardiac troponin I phosphorylation;Ward DG;J Biol Chem,2002

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