ArticleThe Journal of biological chemistry2009
Sites of intra- and intermolecular cross-linking of the N-terminal extension of troponin I in human cardiac whole troponin complex.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Desensitization of the Cardiac Troponin Complex by TnI Phosphorylation and Epigallocatechin-3-Gallate.ACS omega · 2026Article
- NHJournal of cellular signaling · 2021Article
- Structural Dynamics of the N-Extension of Cardiac Troponin I Complexed with Troponin C by Site-Directed Spin Labeling Electron Paramagnetic Resonance.Scientific reports · 2019Article
- Effects of Cardiac Troponin I Mutation P83S on Contractile Properties and the Modulation by PKA-Mediated Phosphorylation.The journal of physical chemistry. B · 2016Article
- Order-Disorder Transitions in the Cardiac Troponin Complex.Journal of molecular biology · 2016Review
- Molecular evolution of troponin I and a role of its N-terminal extension in nematode locomotion.Cytoskeleton (Hoboken, N.J.) · 2016Article
- Myofilament Calcium Sensitivity: Mechanistic Insight into TnI Ser-23/24 and Ser-150 Phosphorylation Integration.Frontiers in physiology · 2016Article
- Troponin I Mutations R146G and R21C Alter Cardiac Troponin Function, Contractile Properties, and Modulation by Protein Kinase A (PKA)-mediated Phosphorylation.The Journal of biological chemistry · 2015Article
- The structural and functional effects of the familial hypertrophic cardiomyopathy-linked cardiac troponin C mutation, L29Q.Journal of molecular and cellular cardiology · 2015Article
- Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24.The Journal of physiology · 2013Article
- New insights into the functional significance of the acidic region of the unique N-terminal extension of cardiac troponin I.Biochimica et biophysica acta · 2013Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
- AMP-activated protein kinase phosphorylates cardiac troponin I at Ser-150 to increase myofilament calcium sensitivity and blunt PKA-dependent function.The Journal of biological chemistry · 2012Article
- The heart-specific NH2-terminal extension regulates the molecular conformation and function of cardiac troponin I.American journal of physiology. Heart and circulatory physiology · 2012Article
- Protein phosphorylation and signal transduction in cardiac thin filaments.The Journal of biological chemistry · 2011Review
- Phosphorylation of cardiac troponin I at protein kinase C site threonine 144 depresses cooperative activation of thin filaments.The Journal of biological chemistry · 2010Article
- Sarcomere control mechanisms and the dynamics of the cardiac cycle.Journal of biomedicine & biotechnology · 2010Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Our previous studies (Howarth, J. W., Meller, J., Solaro, R. J., Trewhella, J., and Rosevear, P. R. (2007) J. Mol. Biol. 373, 706-722) of the unique N-terminal region of human cardiac troponin I (hcTnI), predicted a possible intramolecular interaction near the basic inhibitory peptide. To explore this possibility, we generated single cysteine mutants (hcTnI-S5C and hcTnI-I19C), which were labeled with the hetero-bifunctional cross-linker benzophenone-4-maleimide. The labeled hcTnI was reconstituted to whole troponin and exposed to UV light to form cross-linked proteins. Reversed-phase high-performance liquid chromatography and SDS-PAGE indicated intra- and intermolecular cross-linking with hcTnC and hcTnT. Moreover, using tandem mass spectrometry and Edman sequencing, specific intramolecular sites of interaction were determined at position Met-154 (I19C mutant) and Met-155 (S5C mutant) of hcTnI and intermolecular interactions at positions Met-47 and Met-80 of hcTnC in all conditions. Even though specific intermolecular cross-linked sites did not differ, the relative abundance of cross-linking was altered. We also measured the Ca(2+)-dependent ATPase rate of reconstituted thin filament-myosin-S1 preparation regulated by either cross-linked or non-labeled troponin. Ca(2+) regulation of the ATPase rate was lost when the Cys-5 hcTnI mutant was cross-linked in the absence of Ca(2+), but only partially inhibited with Cys-19 cross-linking in either the presence or absence of Ca(2+). This result indicates different functional effects of cross-linking to Met-154 and Met-155, which are located on different sides of the hcTnI switch peptide. Our data provide novel evidence identifying interactions of the hcTnI-N terminus with specific intra- and intermolecular sites.
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