Editorial
Copyright ©2012 Baishideng.
World J Hypertens. Apr 23, 2012; 2(2): 22-28
Published online Apr 23, 2012. doi: 10.5494/wjh.v2.i2.22
Table 1 The interaction partners with TNNI3K
Putative partnersEffects of the interaction on cardiac systemRef.
Cardiac troponin ITo suppress the phosphorylation of cTnI and increase cardiac functionsZhao et al[1], 2003
Lai et al[4], 2008
Antioxidant protein 1To suppress TNNI3K activity through binding to the sides of ankyrin motif or protein kinase domain of TNNI3KFeng et al[8], 2007
Cardiac α-actin(in)To increase expression of α-actininZhao et al[1], 2003
Lai et al[4], 2008
Endothelin-1To increase endothelin-1-induced cardiomyocytes hypertrophyWang et al[5], 2011
CalsequestrinTo impair systolic contract function and reduce animal survivalWheeler et al[6], 2009
MADS-box factor myocyte enhancer factor-2 (Mef2c)To down-regulate TNNI3K transcription levelWang et al[7], 2008
Cardiac myosin binding protein CUnconfirmedZhao et al[1], 2003
Adult skeletal muscle α-actinUnconfirmedZhao et al[1], 2003
Arylhydrocarbon receptor-interacting proteinUnconfirmedZhao et al[1], 2003
Fatty acid binding protein 3 of heartUnconfirmedZhao et al[1], 2003
Trifunctional enzyme -subunit, mitochondrial precursorUnconfirmedZhao et al[1], 2003