ArticleThe Journal of physiology2011
Mechanism of auxiliary β-subunit-mediated membrane targeting of L-type (Ca(V)1.2) channels.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Molecular Partners of Voltage-Gated Calcium Channel β and αThe Journal of membrane biology · 2026Review
- Degradation of voltage-gated calcium channels: mechanisms and applications in neurological and cardiovascular diseases.Cell communication and signaling : CCS · 2025Review
- Electrosome assembly: Structural insights from high voltage-activated calcium channel (CaV)-chaperone interactions.Biochemical Society transactions · 2025Review
- 14-3-3 promotes sarcolemmal expression of cardiac CaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic Code Expansion for Mechanistic Studies in Ion Channels: An (Un)natural Union of Chemistry and Biology.Chemical reviews · 2024Review
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels.Cell reports · 2024Article
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated CabioRxiv : the preprint server for biology · 2023Article
- Dysregulated Rbfox2 produces aberrant splicing of CaCardiovascular diabetology · 2023Article
- EMC chaperone-CaNature · 2023Article
- Selective posttranslational inhibition of CaNature communications · 2022Article
- Calcium current modulation by the γ1 subunit depends on alternative splicing of CaV1.1.The Journal of general physiology · 2022Article
- Role of High Voltage-Gated CaCells · 2021Review
- Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021Review
- The life cycle of voltage-gated CaNeuronal signaling · 2021Review
- Neuronal junctophilins recruit specific CaeLife · 2021Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- Article
- Cardiac CaV1.2 channels require β subunits for β-adrenergic-mediated modulation but not trafficking.The Journal of clinical investigation · 2019Article
- Regulation of Blood Pressure by Targeting CaCirculation · 2018Article
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Ca(2+) influx via Ca(V)1/Ca(V)2 channels drives processes ranging from neurotransmission to muscle contraction. Association of a pore-forming α(1) and cytosolic β is necessary for trafficking Ca(V)1/Ca(V)2 channels to the cell surface through poorly understood mechanisms. A prevalent idea suggests β binds the α(1) intracellular I-II loop, masking an endoplasmic reticulum (ER) retention signal as the dominant mechanism for Ca(V)1/Ca(V)2 channel membrane trafficking. There are hints that other α(1) subunit cytoplasmic domains may play a significant role, but the nature of their potential contribution is unclear. We assessed the roles of all intracellular domains of Ca(V)1.2-α(1C) by generating chimeras featuring substitutions of all possible permutations of intracellular loops/termini of α(1C) into the β-independent Ca(V)3.1-α(1G) channel. Surprisingly, functional analyses demonstrated α(1C) I-II loop strongly increases channel surface density while other cytoplasmic domains had a competing opposing effect. Alanine-scanning mutagenesis identified an acidic-residue putative ER export motif responsible for the I-II loop-mediated increase in channel surface density. β-dependent increase in current arose as an emergent property requiring four α(1C) intracellular domains, with the I-II loop and C-terminus being essential. The results suggest β binding to the α(1C) I-II loop causes a C-terminus-dependent rearrangement of intracellular domains, shifting a balance of power between export signals on the I-II loop and retention signals elsewhere.
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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.