ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Inhibition of recombinant N-type Ca(V) channels by the gamma 2 subunit involves unfolded protein response (UPR)-dependent and UPR-independent mechanisms.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- N-Type Ca Channel in Epileptic Syndromes and Epilepsy: A Systematic Review of Its Genetic Variants.International journal of molecular sciences · 2023Pooled it
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Identification of Dp140 and α1-syntrophin as novel molecular interactors of the neuronal CaPflugers Archiv : European journal of physiology · 2023Article
- Molecular cloning of the gene promoter encoding the human CaFrontiers in physiology · 2023Article
- Ion channel long non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2022Review
- Expression of tiRNA and tRF inAnnals of translational medicine · 2021Article
- Tetraspanin-7 regulation of L-type voltage-dependent calcium channels controls pancreatic β-cell insulin secretion.The Journal of physiology · 2020Article
- Article
- Trafficking of neuronal calcium channels.Neuronal signaling · 2017Review
- Structure-function of proteins interacting with the α1 pore-forming subunit of high-voltage-activated calcium channels.Frontiers in physiology · 2014Review
- Regulation of high-voltage-activated CaWiley interdisciplinary reviews. Membrane transport and signaling · 2013Article
- Isolation and characterization of the 5´-upstream region of the human voltage-gated Ca(2+) channel α 2δ-1 auxiliary subunit gene: promoter analysis and regulation by transcription factor Sp1.Pflugers Archiv : European journal of physiology · 2013Article
- Genetic basis of pain variability: recent advances.Journal of medical genetics · 2012Review
- Functional coupling of Rab3-interacting molecule 1 (RIM1) and L-type Ca2+ channels in insulin release.The Journal of biological chemistry · 2011Article
- Susceptibility to chronic pain following nerve injury is genetically affected by CACNG2.Genome research · 2010Article
- Stargazin modulates neuronal voltage-dependent Ca(2+) channel Ca(v)2.2 by a Gbetagamma-dependent mechanism.The Journal of biological chemistry · 2010Article
- The GPA-dependent, spherostomatocytosis mutant AE1 E758K induces GPA-independent, endogenous cation transport in amphibian oocytes.American journal of physiology. Cell physiology · 2010Article
- The alpha(2)delta subunit augments functional expression and modifies the pharmacology of Ca(V)1.3 L-type channels.Cell calcium · 2009Article
- The stargazin-related protein gamma 7 interacts with the mRNA-binding protein heterogeneous nuclear ribonucleoprotein A2 and regulates the stability of specific mRNAs, including CaV2.2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- gamma1-dependent down-regulation of recombinant voltage-gated Ca2+ channels.Cellular and molecular neurobiology · 2007Article
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Auxiliary gamma subunits are an important component of high-voltage-activated calcium (Ca(V)) channels, but their precise regulatory role remains to be determined. In the current report, we have used complementary approaches including molecular biology and electrophysiology to investigate the influence of the gamma subunits on neuronal Ca(V) channel activity and expression. We found that coexpression of gamma2 or gamma3 subunits drastically inhibited macroscopic currents through recombinant N-type channels (Ca(V)2.2/beta3/alpha2delta) in HEK-293 cells. Using inhibitors of internalization, we found that removal of functional channels from the plasma membrane is an improbable mechanism of current regulation by gamma. Instead, changes in current amplitude could be attributed to two distinct mechanisms. First, gamma subunit expression altered the voltage dependence of channel activity. Second, gamma subunit expression reduced N-type channel synthesis via activation of the endoplasmic reticulum unfolded protein response. Together, our findings (1) corroborate that neuronal gamma subunits significantly downregulate Ca(V)2.2 channel activity, (2) uncover a role for the gamma2 subunit in Ca(V)2.2 channel expression through early components of the biosynthetic pathway, and (3) suggest that, under certain conditions, channel protein misfolding could be induced by interactions with the gamma subunits, supporting the notion that Ca(V) channels constitute a class of difficult-to-fold proteins.
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