1. Time-dependent cTnI breakdown occurs during global ischemia independent of reperfusion. cTnI breakdown during ischemia is further increased in presence of antioxidants. ROS generated during ischemia may play cTnI protective role. PMID: 15142843
2. cardiac Troponin I Thr144 plays an important role in the acute acceleration of relaxation, whereas Ser23/Ser24 contributes to relaxation during more prolonged activation of protein kinase C by endothelin PMID: 16236710
3. GATA elements control repression of cTNI promoter activity in skeletal muscle cells. PMID: 17875210
4. Overexpression of heat shock protein 27 protects against ischaemia/reperfusion-induced cardiac dysfunction via stabilization of troponin I and T. PMID: 18397962
5. cTnI-R145G expression influences the response to adrenergic stimulation dependent on the receptor subtype PMID: 18548271
6. Metabolic inhibition of cardiomyocytes induces a parallel release of intact cTnI and its degradation products, starting only after onset of irreversible cardiomyocyte damage. PMID: 18721805
7. the nNOS-PMCA4b complex regulates contractility via cAMP and phosphorylation of both PLB and cTnI. PMID: 19278978
8. Data show that dual expression of two CM mutants, tropomyosin mutant A63V and cardiac troponin mutant R146G, were shown to additively slow myocyte relaxation beyond either mutant studied in isolation. PMID: 20161772
9. Ulinastatin may protect myocardium from the damage resulted from sepsis in a rat model, probably by lowering expressions of cTnI, TNF-alpha and ET-1. PMID: 20594472
10. Aan increase in calpain activity may enhance cTnI degradation in the myocardium of tail-suspended rats. PMID: 20945043
11. Cardiac function and phosphorylation of PLB and cTnI were compared in pacing, isoproterenol treatment, and combined pacing and isoproterenol treatment in isolated working heart. PMID: 21876643
12. PKC phosphorylation of cTnI may be maladaptive and potentially associated with cardiac dysfunction PMID: 22052912
13. Structural dynamics of C-domain of cardiac troponin I protein in reconstituted thin filament. PMID: 22207765
14. cTnC, cTnI, cTnT and cTm are not only present in myofilaments of ventricular cardiomyocytes in culture but are also within their nuclei; significantly, these four proteins appear between days 3 and 5 in both myofilaments and nuclei PMID: 22364878
15. differential histidine ionization may be necessary for cTnI A164H to act as a molecular sensor capable of modulating sarcomere performance in response to changes in the cytosolic milieu PMID: 22500757
16. the functional impact of cardiac troponin I (cTnI) phosphorylation by protein kinase A PMID: 22684024
17. Normal developing myocardium and skeletal muscle transiently share both sk-fMHC and cTn-I proteins. PMID: 22808244
18. Hypertrophic cardiomyopathy related mutations R146G/Q and R163W impact interactions between cTnI and cardiac troponin C or actin. PMID: 23246786
19. Mutation in the C helix of cTnC can reduce Ca2+ binding affinity and cTnC-cTnI interaction. PMID: 23454346
20. A cutoff value of 4.8ng/mL for cTnI could be used as early as 8h after MI to accurately identify infarct in this model, whereas echocardiographic images taken 48h after MI predicted the infarcted area 14days after MI. PMID: 23764111
21. Data indicate that the serum TnI level was significantly greater in the acute coronary syndrome (ACS) group compared to the control group. PMID: 23904327
22. molecular determinants of cardiac myocyte performance as conferred by isoform-specific TnI residues PMID: 24853739
23. The findings elucidate the pathogenesis of MI, and the gradual increase in serum adropin could be a novel diagnostic marker and serve as an alternative to troponin-I measurement for diagnosing MI. PMID: 24932661
24. Arsenic induced ventricular hypertrophy occurs via MEF2A/CAMKK2/CALM3/TNNI3 signaling. PMID: 25089838
25. Results suggest that weakened troponin C interaction with cTnI, via PKA phosphorylation of cTnI, may slow thin filament activation and result in increased myofilament relaxation kinetics PMID: 25185555
26. The present study utilizes viral gene transfer of cTnI with phosphomimetic S43D and/or S45D substitutions to evaluate their individual and combined influences on function in intact adult cardiac myocytes. PMID: 25481661
27. This study suggests that cTnI point of care tests can accurately determine heat stroke (HS) severity and could serve as simple, portable, cost-effective HS field tests. PMID: 26290107
28. cTnIS43/45N is a functionally conservative substitution, and may be appropriate for use as a phospho-null in rodent models designed for studies on PKC modulation of cardiac performance PMID: 26869200
29. the interaction between cTnC and cTnI in skinned papillary muscle strips is dependent on sarcomere length PMID: 26944554
30. Cardiac troponin I mutation P83S present in hypertrophic cardiomyopathy changes the contractile myofibril properties and modulation by PKA-mediated phosphorylation. PMID: 27150586
31. These findings demonstrate that S-nitrosylation and S-glutathionylation exert opposing effects on Ca(2+) sensitivity in mammalian FT muscle fibers, mediated by competitive actions on Cys134 of TnIf. PMID: 27974300
32. PKC phosphorylates cardiac troponin I (cTnI) S23/24, S43/45 and T144 to fine tune myocyte function. PMID: 28587770
33. Troponin I interaction with calcium and Troponin C in cardiac muscle PMID: 28864299
34. Compared to cTnI(WT), both truncations displayed greater Ca(2+)-sensitivity and faster cross-bridge attachment rates at both SLs. Furthermore, cTnI(1-167) slowed MgADP release rate and enhanced cross-bridge binding. Our findings imply that cTnI-MD truncations affect the blocked-to closed-state transition(s) and destabilize the closed-state position of tropomyosin. PMID: 28958680
35. Pim-1 is a novel kinase that phosphorylates cTnI primarily at Ser23/24 and Ser150 in cardiomyocytes, which in turn may modulate myofilament function under a variety of physiological and pathophysiological conditions. PMID: 29544221

KEGG: rno:29248

STRING: 10116.ENSRNOP00000024640

UniGene: Rn.64141