ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Modulation of the cloned skeletal muscle L-type Ca2+ channel by anchored cAMP-dependent protein kinase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 90 citations in OpenAlex.
- Effects of adrenaline on contractility and endurance of isolated mammalian soleus with different calcium concentrations.Journal of muscle research and cell motility · 2019Article
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- Protein phosphorylation maintains the normal function of cloned human CaThe Journal of general physiology · 2018Article
- Apparent lack of physical or functional interaction between CaV1.1 and its distal C terminus.The Journal of general physiology · 2015Article
- Stac adaptor proteins regulate trafficking and function of muscle and neuronal L-type Ca2+ channels.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Regulation of Cardiac Calcium Channels in the Fight-or-Flight Response.Current molecular pharmacology · 2015Review
- Regulation of voltage-gated calcium channels by proteolysis.Sheng li xue bao : [Acta physiologica Sinica] · 2012Review
- Voltage-gated calcium channels.Cold Spring Harbor perspectives in biology · 2011Review
- Signaling complexes of voltage-gated sodium and calcium channels.Neuroscience letters · 2010Review
- In vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.The Journal of physiology · 2010Article
- Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.The Journal of physiology · 2009Article
- Supramolecular assemblies and localized regulation of voltage-gated ion channels.Physiological reviews · 2009Review
- Arachidonate-regulated Ca2+-selective (ARC) channel activity is modulated by phosphorylation and involves an A-kinase anchoring protein.The Journal of physiology · 2005Article
- Sites of proteolytic processing and noncovalent association of the distal C-terminal domain of CaV1.1 channels in skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Convergent regulation of skeletal muscle Ca2+ channels by dystrophin, the actin cytoskeleton, and cAMP-dependent protein kinase.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Direct and remote modulation of L-channels in chromaffin cells: distinct actions on alpha1C and alpha1D subunits?Molecular neurobiology · 2004Review
- Beta subunits of voltage-gated calcium channels.Journal of bioenergetics and biomembranes · 2003Review
- Beta-adrenergic regulation requires direct anchoring of PKA to cardiac CaV1.2 channels via a leucine zipper interaction with A kinase-anchoring protein 15.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Skeletal muscle L-type Ca(2+) current modulation in gamma1-deficient and wildtype murine myotubes by the gamma1 subunit and cAMP.The Journal of physiology · 2002Article
- Protein kinase modulation of a neuronal cation channel requires protein-protein interactions mediated by an Src homology 3 domain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ influx through skeletal muscle Ca2+ channels and the force of contraction are increased in response to beta-adrenergic stimulation and high-frequency electrical stimulation. These effects are thought to be mediated by cAMP-dependent phosphorylation of the skeletal muscle Ca2+ channel. Modulation of the cloned skeletal muscle Ca2+ channel by cAMP-dependent phosphorylation and by depolarizing prepulses was reconstituted by transient expression in tsA-201 cells and compared to modulation of the native skeletal muscle Ca2+ channel as expressed in mouse 129CB3 skeletal muscle cells. The heterologously expressed Ca2+ channel consisting of alpha1, alpha2delta, and beta subunits gave currents that were similar in time course, current density, and dihydropyridine sensitivity to the native Ca2+ channel. cAMP-dependent protein kinase (PKA) stimulation by Sp-5,6-DCl-cBIMPS (cBIMPS) increased currents through both native and expressed channels two- to fourfold. Tail currents after depolarizations to potentials between -20 and +80 mV increased in amplitude and decayed more slowly as either the duration or potential of the depolarization was increased. The time- and voltage-dependent slowing of channel deactivation required the activity of PKA, because it was enhanced by cBIMPS and reduced or eliminated by the peptide PKA inhibitor PKI (5-24) amide. This voltage-dependent modulation of the cloned skeletal muscle Ca2+ channel by PKA also required anchoring of PKA by A-Kinase Anchoring Proteins because it was blocked by peptide Ht 31, which disrupts such anchoring. The results show that the skeletal muscle Ca2+ channel expressed in heterologous cells is modulated by PKA at rest and during depolarization and that this modulation requires anchored protein kinase, as it does in native skeletal muscle cells.
Indexed as
Identifiers
9006969PMC6793735W1590554196What OpenQuestion holds
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.