ArticleJournal of biomedicine & biotechnology2011
The IQ motif is crucial for Cav1.1 function.
Article in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Crystal Structure of Calmodulin Bound to the Cardiac Ryanodine Receptor (RyR2) at Residues Phe4246-Val4271 Reveals a Fifth Calcium Binding Site.Biochemistry · 2021Article
- Calmodulin-Binding Proteins in Muscle: A Minireview on Nuclear Receptor Interacting Protein, Neurogranin, and Growth-Associated Protein 43.International journal of molecular sciences · 2020Review
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- STAC proteins associate to the IQ domain of CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Evidence for Altered CaFrontiers in physiology · 2016Article
- Calmodulin regulation (calmodulation) of voltage-gated calcium channels.The Journal of general physiology · 2014Review
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Authors and funding
1 author.
Funding
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Abstract
Ca(2+)-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca(2+) channels. The skeletal muscle Ca(v)1.1 also exhibits Ca(2+)-/CaM-dependent modulation. Here, whole-cell Ca(2+) current, Ca(2+) transient, and maximal, immobilization-resistant charge movement (Q(max)) recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Ca(v)1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Ca(v)1.1 was examined. In dysgenic myotubes expressing YFP-Ca(v)1.1(AA), neither Ca(2+) currents nor evoked Ca(2+) transients were detectable. The loss of Ca(2+) current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. The Q(max) in dysgenic myotubes expressing YFP-Ca(v)1.1(AA) was similar to that of normal myotubes. These findings suggest that the IQ motif of the Ca(v)1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR.
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