BACKGROUND Troponin I (TnI), along with Troponin T (TnT) and Troponin C (TnC), is one of 3 subunits that form the Troponin complex of the thin filaments of striated muscle, which confers calcium-sensitivity to striated muscle actomyosin ATPase activity. TnI is the inhibitory subunit; blocking actin-myosin interactions and thereby mediating striated muscle relaxation. The TnI subfamily contains three genes: TnI-skeletal-fast-twitch, TnI-skeletal-slow-twitch, and TnI-cardiac. cTnI gene encodes the TnI-cardiac protein and is exclusively expressed in cardiac muscle tissues. Mutations in cTnI gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM).1
There is evidence for PKC and PKA-dependent multisite phosphorylation of cardiac troponin I (cTnI) at Ser-23 and Ser-24 (also PKA sites) in the cardiac-specific N-terminal extension and at Thr-144, a unique residue in the inhibitory region.2,3 p90RSK is also involved in this phosphorylation process.2 The functional effect of these phosphorylations may be involved in regulation of intramolecular interaction between the N-terminal extension and the inhibitory region of cTnI and depress the acto-myosin interaction. It may be important during the progression of heart failure.
1. Sleeper, M.M. et al:J. Veterin. Intern Med. 15:501-3, 2008
2. Itoh, S. et al: J. Biol. Chem. 280:24135-42, 2005
3. Chandra, M. et al: Biochem. 36:13305-11, 1997
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