ArticleJournal of muscle research and cell motility2005
Possible functions of p94 in connectin-mediated signaling pathways in skeletal muscle cells.
Article in Journal of muscle research and cell motility, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 41 citations in OpenAlex.
- Urinary N-terminal titin fragment ascertained as biomarker in a small cohort of limb-girdle muscular dystrophy LGMDR1-calpain 3 related.Journal of neuromuscular diseases · 2025Article
- CAPN3: A muscle‑specific calpain with an important role in the pathogenesis of diseases (Review).International journal of molecular medicine · 2021Review
- Perturbation of the titin/MURF1 signaling complex is associated with hypertrophic cardiomyopathy in a fish model and in human patients.Disease models & mechanisms · 2019Article
- Z-band and M-band titin splicing and regulation by RNA binding motif 20 in striated muscles.Journal of cellular biochemistry · 2018Article
- Translocation of molecular chaperones to the titin springs is common in skeletal myopathy patients and affects sarcomere function.Acta neuropathologica communications · 2017Article
- Interactions with M-band titin and calpain 3 link myospryn (CMYA5) to tibial and limb-girdle muscular dystrophies.The Journal of biological chemistry · 2010Article
- Muscle giants: molecular scaffolds in sarcomerogenesis.Physiological reviews · 2009Review
- Cytoplasmic Ig-domain proteins: cytoskeletal regulators with a role in human disease.Cell motility and the cytoskeleton · 2009Review
- Endogenous calpain-3 activation is primarily governed by small increases in resting cytoplasmic [Ca2+] and is not dependent on stretch.The Journal of biological chemistry · 2009Article
- Calpain 3, the "gatekeeper" of proper sarcomere assembly, turnover and maintenance.Neuromuscular disorders : NMD · 2008Review
- Muscle-specific calpain is localized in regions near motor endplates in differentiating lobster claw muscles.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2007Article
- [Cellular regulation of anabolism and catabolism in skeletal muscle during immobilisation, aging and critical illness].Wiener klinische Wochenschrift · 2007Review
- Screening of calpain-3 autolytic activity in LGMD muscle: a functional map of CAPN3 gene mutations.Journal of medical genetics · 2007Article
- Ca2+ activation of diffusible and bound pools of mu-calpain in rat skeletal muscle.The Journal of physiology · 2006Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calpains are intracellular Ca2+ -requiring 'modulator proteases', which modulate cellular functions by limited and specific proteolysis. p94/calpain3, a skeletal-muscle specific calpain, has been one of the representative calpain species which indicates physiological importance of calpain proteolytic system; a defect of proteolytic activity of p94 causes limb girdle muscular dystrophy type2A (LGMD2A, also called 'calpainopathy'). Immunohistochemical studies on myofibrils showed that p94 localizes at the Z- and N2-line regions of sarcomeres. It was also identified by the yeast two hybrid studies that p94 binds to the N2A and M-line regions of connectin. Furthermore, genetic studies indicate that p94 is indispensable for skeletal muscles, although its precise functions are still unclear. Interestingly, connectin provides sarcomere not only with elasticity but also with binding sites to various multi-functional proteins such as muscle ankyrin repeat proteins (MARPs), muscle RING finger proteins (MURFs), titin-capping protein (T-cap/telethonin), sarcomeric-alpha-actinin, p94 etc. Binding sites for these proteins are not randomly placed along connectin but rather accumulated in the Z-, N2-, and/or M-line regions, indicating the existence of 'signal complexes' unique to each regions. The concept of these complexes are strongly supported by the facts that mutations of connectin or its binding proteins in these regions severely perturb muscle functions, as in the case of LGMD2A caused by mutations in the p94 gene. Therefore, it is hypothesized that the 'signal complexes' in the Z-, N2-, and M-lines modulate muscle cell homeostasis by transducing signals of external stimulations/stresses to trigger appropriate response at various different cellular events such as protein modification and gene expressions. In this article, we performed detailed immunohistochemical analyses of p94 on isolated single myofibers. Together with recent findings about p94, it is suggested that sarcomeric localization of p94, especially its M-line localization, is affected by the combination of cellular contexts such as contractile status of myofibrils, fiber type compositions, sarcomeric maturation, and the composition of the 'signal complexes' in each region.
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