ArticleJournal of molecular and cellular cardiology2010
Why does troponin I have so many phosphorylation sites? Fact and fancy.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
- Altering Calcium Sensitivity in Heart Failure: A Crossroads of Disease Etiology and Therapeutic Innovation.International journal of molecular sciences · 2023Review
- Mouse Models of Cardiomyopathies Caused by Mutations in Troponin C.International journal of molecular sciences · 2023Review
- Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model.ESC heart failure · 2022Article
- Current Understanding of Molecular Pathophysiology of Heart Failure With Preserved Ejection Fraction.Frontiers in physiology · 2022Review
- Calcium Buffering in the Heart in Health and Disease.Circulation · 2019Review
- Cardiac troponins may be irreversibly modified by glycation: novel potential mechanisms of cardiac performance modulation.Scientific reports · 2018Article
- Top-down Proteomics: Technology Advancements and Applications to Heart Diseases.Expert review of proteomics · 2016Review
- TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Gene · 2016Review
- Review
- Pathomechanisms in heart failure: the contractile connection.Journal of muscle research and cell motility · 2015Review
- Dissociation of Calcium Transients and Force Development following a Change in Stimulation Frequency in Isolated Rabbit Myocardium.BioMed research international · 2015Article
- Distinct conformational and functional effects of two adjacent pathogenic mutations in cardiac troponin I at the interface with troponin T.FEBS open bio · 2015Article
- The cardiac-specific N-terminal region of troponin I positions the regulatory domain of troponin C.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Top-down proteomics reveals concerted reductions in myofilament and Z-disc protein phosphorylation after acute myocardial infarction.Molecular & cellular proteomics : MCP · 2014Article
- Troponin I phosphorylation in human myocardium in health and disease.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
- Long term ablation of protein kinase A (PKA)-mediated cardiac troponin I phosphorylation leads to excitation-contraction uncoupling and diastolic dysfunction in a knock-in mouse model of hypertrophic cardiomyopathy.The Journal of biological chemistry · 2014Article
- Signaling by S-nitrosylation in the heart.Journal of molecular and cellular cardiology · 2014Review
- Top-down mass spectrometry of cardiac myofilament proteins in health and disease.Proteomics. Clinical applications · 2014Review
- Single acute stress-induced progesterone and ovariectomy alter cardiomyocyte contractile function in female rats.Croatian medical journal · 2014Article
- Proteomics in heart failure: top-down or bottom-up?Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
We discuss a current controversy regarding the relative role of phosphorylation sites on cardiac troponin I (cTnI) (Fig. 1) in physiological and patho-physiological cardiac function. Studies with mouse models and in vitro studies indicate that multi-site phosphorylations are involved in both control of maximum tension and sarcomeric responsiveness to Ca(2+). Thus one hypothesis is that cardiac function reflects a balance of cTnI phosphorylations and a tilt in this balance may be maladaptive in acquired and genetic disorders of the heart. Studies on human heart samples taken mainly at end-stage heart failure, and in depth proteomic analysis of human and rat heart samples demonstrate that Ser23/Ser24 are the major and perhaps the only sites likely to be relevant to control cardiac function. Thus functional significance of Ser23/Ser24 phosphorylation is taken as fact, whereas the function of some other sites is treated as fancy. Maybe the extremes will meet: in any case we both agree that further work needs to be carried out with relatively large mammals and with determination of the time course of changes in phosphorylation to identify transient modifications that may be relevant at a beat-to-beat basis. Moreover, we agree that the changes and effects of cTnI phosphorylation need to be fully integrated into the effects of other phosphorylations in the cardiac myocyte.
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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.