ArticleJournal of muscle research and cell motility2006
A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I.
Article in Journal of muscle research and cell motility, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Assessing Cardiac Contractility From Single Molecules to Whole Hearts.JACC. Basic to translational science · 2024Review
- Cell biology of sarcomeric protein engineering: disease modeling and therapeutic potential.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- Synchronous in situ ATPase activity, mechanics, and Ca2+ sensitivity of human and porcine myocardium.Biophysical journal · 2009Article
- Impaired relaxation is the main manifestation in transgenic mice expressing a restrictive cardiomyopathy mutation, R193H, in cardiac TnI.American journal of physiology. Heart and circulatory physiology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to incorporate human cardiac troponin I (TnI) and troponin C (TnC) into guinea pig skinned cardiac trabeculae, fibres were treated with vanadate to extract endogenous TnI and TnC using established protocols. After addition of human TnI and TnC force was inadequately restored and it was found that the vanadate treatment had unexpectedly also removed some troponin T. To recover Ca(2+)-sensitive force, the fibres had to be incubated with all three troponin subunits. Using this revised method, the hypertrophic cardiomyopathy-causing mutation TnI Gly203Ser had no significant effect on Ca(2+)-sensitivity of force production, contrasting with our earlier report of decreased Ca(2+)-sensitivity which was likely caused by the unexpectedly harsh effect of vanadate.
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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.