ArticleJournal of muscle research and cell motility1996
Quantitative analysis of low molecular weight G-actin-binding proteins, cofilin, ADF and profilin, expressed in developing and degenerating chicken skeletal muscles.
Article in Journal of muscle research and cell motility, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 35 citations in OpenAlex.
- DNA-PKcs Phosphorylates Cofilin2 to Induce Endothelial Dysfunction and Microcirculatory Disorder in Endotoxemic Cardiomyopathy.Research (Washington, D.C.) · 2024Article
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- Alterations in thin filament length during postnatal skeletal muscle development and aging in mice.Frontiers in physiology · 2014Article
- Functions of cofilin in cell locomotion and invasion.Nature reviews. Molecular cell biology · 2013Review
- Dynamic regulation of sarcomeric actin filaments in striated muscle.Cytoskeleton (Hoboken, N.J.) · 2010Review
- The full length cloning of a novel porcine gene CFL2b and its influence on the MyHC expression.Molecular biology reports · 2009Article
- Activity of cofilin can be regulated by a mechanism other than phosphorylation/dephosphorylation in muscle cells in culture.Journal of muscle research and cell motility · 2007Article
- Cofilin and DNase I affect the conformation of the small domain of actin.Biophysical journal · 2002Article
- The Caenorhabditis elegans unc-78 gene encodes a homologue of actin-interacting protein 1 required for organized assembly of muscle actin filaments.The Journal of cell biology · 2001Article
- UNC-60B, an ADF/cofilin family protein, is required for proper assembly of actin into myofibrils in Caenorhabditis elegans body wall muscle.The Journal of cell biology · 1999Article
- Organization of connectin/titin filaments in sarcomeres of differentiating chicken skeletal muscle cells.Molecular and cellular biochemistry · 1999Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large amount of G-actin is pooled in the cytoplasm of young embryonic skeletal muscle and, although its concentration is reduced as muscle develops, the total amount of actin in muscle cells increases remarkably. Three G-actin-binding proteins, cofilin, ADF and profilin, are known to be involved in creating the G-actin pool in the embryonic muscle. To better understand how they are responsible for the regulation of assembly and disassembly of actin in developing and degenerating muscles, we measured the amounts of the three G-actin-binding proteins by means of quantitative immunoblotting and compared them with that of G-actin. The sum of the amounts of the three actin-binding proteins was insufficient at early developmental stages but sufficient at later stages to account for the pool of G-actin in young muscle cells. It decreased in parallel with the decrease in the G-actin pool as muscle developed. Expression of thymosin beta 4, which is known to be extremely important for G-actin-sequestering in a variety of non-muscle cells, was detected at a considerable level in young embryonic but not in adult skeletal muscles according to Northern and Western blotting. In degenerating denervated and dystrophic muscles, cofilin and profilin, but not ADF, were significantly increased in amount. From these results, we conclude that the G-actin pool in young embryonic skeletal muscle is mainly due to cofilin, ADF, profilin and thymosin beta 4, but thymosin beta 4 as well as ADF becomes less important as muscle develops. Cofilin and profilin may also be involved in the redistribution of actin during myofibrillogenesis and in the process of actin disassembly in degenerating muscles.
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