motifs/domains
| 12-residue alpha-helix at the N terminus, EF-hand loop (NH2-DEDGSGTVDFDE-COOH) with six residues (bold) that coordinate Ca2+ binding and six residues that do not appear to influence Ca2+ binding directly  |
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the N helix, containing Ca++ binding site, that responds to Ca2+ to regulate muscle contraction, and N terminus plays an important role in the regulation of cardiac muscle contraction by moving the C-terminal region of TNNI3 from its actin-binding inhibitory location and enhancing the movement of tropomyosin away from its inhibitory position |
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two globular EF-hand domains connected by a flexible linker |
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a C-domain sites that are thought to be permanently occupied by Ca2+ and/or Mg2+, thus playing a structural role by anchoring TNNC1 into the thin filament (Swindle 2010), and Ca(2+)/Mg(2+) sites (III and IV) modulate crossbridge-mediated thin filament activation in cardiac myofibrils |
| basic FUNCTION
| preventing actin and myosin interaction in resting muscle tissue |
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involved in regulation of striated muscle contraction |
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its Ca(2+) binding properties modulate the rate of cardiac muscle contraction at submaximal levels of Ca(2+) activation |
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is required both for the function and structural integrity of the contractile machinery in cardiomyocytes |
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important regulatory molecule in cardiomyocytes |
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may act as a hub, sensing physiological and pathological stimuli to modulate the Ca(2+)-binding properties of the thin filament and influence the contractile performance of the heart |
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calcium-binding subunit of the troponin complex responsible for initiating striated muscle contraction in response to calcium influx |
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Ca2+ sensor and key regulator of contraction |
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role of TNNC1 mutations in the development of cardiomyopathy |
