ArticleBiophysical journal2001
Ca2+ - and cross-bridge-dependent changes in N- and C-terminal structure of troponin C in rat cardiac muscle.
Article in Biophysical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- The structure of the native cardiac crossbridge in the rigor state.Science advances · 2026Article
- The force of the myosin motor sets cooperativity in thin filament activation of skeletal muscles.Communications biology · 2022Article
- Actomyosin Complex.Sub-cellular biochemistry · 2022Article
- The structure of the native cardiac thin filament at systolic CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- Effects of Cardiac Troponin I Mutation P83S on Contractile Properties and the Modulation by PKA-Mediated Phosphorylation.The journal of physical chemistry. B · 2016Article
- Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility.Archives of biochemistry and biophysics · 2016Review
- 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
- PKA phosphorylation of cardiac troponin I modulates activation and relaxation kinetics of ventricular myofibrils.Biophysical journal · 2014Article
- Structural and functional consequences of cardiac troponin C L57Q and I61Q Ca(2+)-desensitizing variants.Archives of biochemistry and biophysics · 2013Article
- Transgenic overexpression of ribonucleotide reductase improves cardiac performance.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Finite Element Estimation of Protein-Ligand Association Rates with Post-Encounter Effects: Applications to Calcium binding in Troponin C and SERCA.Computational science & discovery · 2012Article
- A mutation in TNNC1-encoded cardiac troponin C, TNNC1-A31S, predisposes to hypertrophic cardiomyopathy and ventricular fibrillation.The Journal of biological chemistry · 2012Article
- Structural and functional consequences of the cardiac troponin C L48Q Ca(2+)-sensitizing mutation.Biochemistry · 2012Article
- Calcium binding kinetics of troponin C strongly modulate cooperative activation and tension kinetics in cardiac muscle.Journal of molecular and cellular cardiology · 2011Article
- The molecular basis of the steep force-calcium relation in heart muscle.Journal of molecular and cellular cardiology · 2010Review
- Cooperative cross-bridge activation of thin filaments contributes to the Frank-Starling mechanism in cardiac muscle.Biophysical journal · 2009Article
- Calcium- and myosin-dependent changes in troponin structure during activation of heart muscle.The Journal of physiology · 2009Article
- The effects of force inhibition by sodium vanadate on cross-bridge binding, force redevelopment, and Ca2+ activation in cardiac muscle.Biophysical journal · 2007Article
- Investigation of thin filament near-neighbour regulatory unit interactions during force development in skinned cardiac and skeletal muscle.The Journal of physiology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Linear dichroism of 5'-tetramethylrhodamine (5'ATR)-labeled cardiac troponin C (cTnC) was measured to monitor cTnC structure during Ca2+-activation of force in rat skinned myocardium. Mono-cysteine mutants allowed labeling at Cys-84 (cTnC(C84), near the D/E helix linker); Cys-35 (cTnC(C35), at nonfunctional site I); or near the C-terminus with a cysteine inserted at site 98 (cTnC-C35S,C84S,S98C, cTnC(C98)). With 5'ATR-labeled cTnC(C84) and cTnC(C98) dichroism increased with increasing [Ca2+], while rigor cross-bridges caused dichroism to increase more with 5'ATR-labeled cTnC(C84) than cTnC(C98). The pCa50 values and n(H) from Hill analysis of the Ca2+-dependence of force and dichroism were 6.4 (+/-0.02) and 1.08 (+/-0.04) for force and 6.3 (+/-0.04) and 1.02 (+/-0.09) (n = 5) for dichroism in cTnC(C84) reconstituted trabeculae. Corresponding data from cTnC(C98) reconstituted trabeculae were 5.53 (+/-0.03) and 3.1 (+/-0.17) for force, and 5.39 (+/-0.03) and 1.87 (+/-0.17) (n = 5) for dichroism. The contribution of active cycling cross-bridges to changes in cTnC structure was determined by inhibition of force to 6% of pCa 4.0 controls with 1.0 mM sodium vanadate (Vi). With 5'ATR-labeled cTnC(C84) Vi caused both the pCa50)of dichroism and the maximum value at pCa 4.0 to decrease, while with 5'ATR-labeled cTnC(C98) the pCa50 of dichroism decreased with no change of dichroism at pCa 4.0. The dichroism of 5'ATR-labeled cTnC(C35) was insensitive to either Ca2+ or strong cross-bridges. These data suggest that both Ca2+ and cycling cross-bridges perturb the N-terminal structure of cTnC at Cys-84, while C-terminal structure is altered by site II Ca2+-binding, but not cross-bridges.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.