ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Solution NMR and calorimetric analysis of Rem2 binding to the Ca2+ channel β4 subunit: a low affinity interaction is required for inhibition of Cav2.1 Ca2+ currents.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- 14-3-3 proteins: Regulators of cardiac excitation-contraction coupling and stress responses.The Journal of physiology · 2026Review
- Molecular Partners of Voltage-Gated Calcium Channel β and αThe Journal of membrane biology · 2026Review
- A membrane-associated phosphoswitch in Rad controls adrenergic regulation of cardiac calcium channels.The Journal of clinical investigation · 2024Article
- Engineering selectivity into RGK GTPase inhibition of voltage-dependent calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The small GTPase RSG1 controls a final step in primary cilia initiation.The Journal of cell biology · 2018Article
- Functional assessment of three Rem residues identified as critical for interactions with Ca(2+) channel β subunits.Pflugers Archiv : European journal of physiology · 2015Article
- The role of auxiliary subunits for the functional diversity of voltage-gated calcium channels.Journal of cellular physiology · 2015Review
- Rem uncouples excitation-contraction coupling in adult skeletal muscle fibers.The Journal of general physiology · 2015Article
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Authors and funding
4 authors.
Funding
Abstract
Rem, Rad, Kir/Gem (RGK) proteins, including Rem2, mediate profound inhibition of high-voltage activated Ca(2+) channels containing intracellular regulatory β subunits. All RGK proteins bind to voltage-gated Ca(2+) channel β subunit (Cavβ) subunits in vitro, but the necessity of the interaction for current inhibition remains controversial. This study applies NMR and calorimetric techniques to map the binding site for Rem2 on human Cavβ4a and measure its binding affinity. Our experiments revealed 2 binding surfaces on the β4 guanylate kinase domain contributing to a 156 ± 18 µM Kd interaction: a hydrophobic pocket lined by 4 critical residues (L173, N261, H262, and V303), mutation of any of which completely disrupted binding, and a nearby surface containing 3 residues (D206, L209, and D258) that when individually mutated decreased affinity. Voltage-gated Ca(2+) channel α1A subunit (Cav2.1) Ca(2+) currents were completely inhibited by Rem2 when co-expressed with wild-type Cavβ4a, but were unaffected by Rem2 when coexpressed with a Cavβ4a site 1 (L173A/V303A) or site 2 (D258A) mutant. These results provide direct evidence for a low-affinity Rem2/Cavβ4 interaction and show definitively that the interaction is required for Cav2.1 inhibition.
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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 Socratic graph.