ArticleThe Journal of physiology2007
Reorganized stores and impaired calcium handling in skeletal muscle of mice lacking calsequestrin-1.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 154 citations in OpenAlex.
- Review
- Review
- Deep-time gene expression shift reveals an ancient change in avian muscle phenotypes.PLoS genetics · 2025Article
- ERG1A KScientific reports · 2025Article
- TAM-associated CASQ1 mutants diminish intracellular CaJournal of muscle research and cell motility · 2024Article
- Aerobic Exercise Modulates Proteomic Profiles in Gastrocnemius Muscle ofLife (Basel, Switzerland) · 2024Article
- Cytosolic CaBiophysical reports · 2023Article
- Article
- Constitutive assembly of Ca2+ entry units in soleus muscle from calsequestrin knockout mice.The Journal of general physiology · 2022Article
- Article
- Store-Operated CaInternational journal of molecular sciences · 2022Article
- Article
- Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022Review
- Ryanodine receptor leak triggers fiber CaScience advances · 2021Article
- Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021Review
- Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.Journal of muscle research and cell motility · 2021Article
- Calsequestrin, a key protein in striated muscle health and disease.Journal of muscle research and cell motility · 2021Review
- Caffeine as a tool to investigate sarcoplasmic reticulum and intracellular calcium dynamics in human skeletal muscles.Journal of muscle research and cell motility · 2021Review
- Pathological mechanisms of vacuolar aggregate myopathy arising from a Casq1 mutation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- A View of the Endoplasmic Reticulum Through the Calreticulin Lens.Progress in molecular and subcellular biology · 2021Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Calsequestrin (CS), the major Ca(2+)-binding protein in the sarcoplasmic reticulum (SR), is thought to play a dual role in excitation-contraction coupling: buffering free Ca(2+) increasing SR capacity, and modulating the activity of the Ca(2+) release channels (RyRs). In this study, we generated and characterized the first murine model lacking the skeletal CS isoform (CS1). CS1-null mice are viable and fertile, even though skeletal muscles appear slightly atrophic compared to the control mice. No compensatory increase of the cardiac isoform CS2 is detectable in any type of skeletal muscle. CS1-null muscle fibres are characterized by structural and functional changes, which are much more evident in fast-twitch muscles (EDL) in which most fibres express only CS1, than in slow-twitch muscles (soleus), where CS2 is expressed in about 50% of the fibres. In isolated EDL muscle, force development is preserved, but characterized by prolonged time-to-peak and half-relaxation time, probably related to impaired calcium release from and re-uptake by the SR. Ca(2+)-imaging studies show that the amount of Ca(2+) released from the SR and the amplitude of the Ca(2+) transient are significantly reduced. The lack of CS1 also causes significant ultrastructural changes, which include: (i) striking proliferation of SR junctional domains; (ii) increased density of Ca(2+)-release channels (confirmed also by (3)H-ryanodine binding); (iii) decreased SR terminal cisternae volume; (iv) higher density of mitochondria. Taken together these results demonstrate that CS1 is essential for the normal development of the SR and its calcium release units and for the storage and release of appropriate amounts of SR Ca(2+).
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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.