Nuclear tropomyosin and troponin in striated muscle: New roles in a new locale?
Journal of Muscle Research and Cell Motility, ISSN: 0142-4319, Vol: 34, Issue: 3-4, Page: 275-284
2013
- 27Citations
- 21Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations27
- Citation Indexes27
- 27
- CrossRef11
- Captures21
- Readers21
- 21
Review Description
Tropomyosin and troponin have well known Ca-regulatory functions in the striated muscle sarcomere. In this review, we summarize experimental evidence that tropomyosin and troponin are localized, with as yet unidentified functional roles, in the striated muscle cell nucleus. We also apply bioinformatics approaches that predict localization of some tropomyosin and troponin to the nucleus, and that SUMOylation could be a covalent modification that modulates their nuclear localization and function. Further, we provide examples of cardiomyopathy mutations that alter the predicted likelihood of nuclear localization and SUMOylation of tropomyosin. These observations suggest novel mechanisms by which cardiomyopathy mutations in tropomyosin and troponin might alter not only cardiac contractility but also nuclear function. © 2013 Springer Science+Business Media Dordrecht.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84890120208&origin=inward; http://dx.doi.org/10.1007/s10974-013-9356-7; http://www.ncbi.nlm.nih.gov/pubmed/23907338; http://link.springer.com/10.1007/s10974-013-9356-7; https://dx.doi.org/10.1007/s10974-013-9356-7; https://link.springer.com/article/10.1007/s10974-013-9356-7
Springer Science and Business Media LLC
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