ArticleAmerican journal of physiology. Cell physiology2009
Properties of easily releasable myofilaments: are they the first step in myofibrillar protein turnover?
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
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- Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.Ageing research reviews · 2021Review
- Breakdown of Filamentous Myofibrils by the UPS-Step by Step.Biomolecules · 2021Review
- Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.Journal of molecular and cellular cardiology · 2020Review
- Impact of porcine reproductive and respiratory syndrome virus on muscle metabolism of growing pigs1.Journal of animal science · 2019Article
- Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Metabolic adaptation of pigs to a Mycoplasma hyopneumoniae and Lawsonia intracellularis dual challenge.Journal of animal science · 2018Article
- Porcine epidemic diarrhea virus reduces feed efficiency in nursery pigs.Journal of animal science · 2018Article
- Skeletal muscle and resistance exercise training; the role of protein synthesis in recovery and remodeling.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Review
- UBE2B is implicated in myofibrillar protein loss in catabolic C2C12 myotubes.Journal of cachexia, sarcopenia and muscle · 2016Article
- Structural and functional changes in the zebrafish (Danio rerio) skeletal muscle after cadmium exposure.Cell biology and toxicology · 2015Article
- Role of E2-Ub-conjugating enzymes during skeletal muscle atrophy.Frontiers in physiology · 2015Review
- Proteomics of muscle chronological ageing in post-menopausal women.BMC genomics · 2014Article
- Inhibition of the ubiquitin-proteasome pathway does not protect against ventilator-induced accelerated proteolysis or atrophy in the diaphragm.Anesthesiology · 2014Article
- Label-free quantitative protein profiling of vastus lateralis muscle during human aging.Molecular & cellular proteomics : MCP · 2014Article
- Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy.The Journal of cell biology · 2012Article
- Myosin heavy chain is not selectively decreased in murine cancer cachexia.International journal of cancer · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Myofibrillar proteins must be removed from the myofibril before they can be turned over metabolically in functioning muscle cells. It is uncertain how this removal is accomplished without disruption of the contractile function of the myofibril. It has been proposed that the calpains could remove the outer layer of filaments from myofibrils as a first step in myofibrillar protein turnover. Several studies have found that myofilaments can be removed from myofibrils by trituration in the presence of ATP. These easily releasable myofilaments (ERMs) were proposed to be intermediates in myofibrillar protein turnover. It was unclear, however, whether the ERMs were an identifiable entity in muscle or whether additional trituration would remove more myofilaments until the myofibril was gone and whether calpains could release ERMs from intact myofibrils. The present study shows that few ERMs could be obtained from the residue after the first removal of ERMs, and the yield of ERMs from well-washed myofibrils was reduced, probably because some ERMs had been removed by the washing process. Mild calpain treatment of myofibrils released filaments that had a polypeptide composition and were ultrastructurally similar to ERMs. The yield of calpain-released ERMs was two- to threefold greater than the normal yield. Hence, ERMs are an identifiable entity in myofibrils, and calpain releases filaments that are similar to ERMs. The role of ERMs in myofibrillar protein turnover is unclear, because only filaments on the surface of the myofibril would turn over, and changes in myofibrillar protein isoforms during development could not occur via the ERM mechanism.
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