ArticleProceedings of the National Academy of Sciences of the United States of America1994
Voltage-dependent potentiation of L-type Ca2+ channels in skeletal muscle cells requires anchored cAMP-dependent protein kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 187 citations in OpenAlex.
- Article
- Insulin-Induced Cardiomyocytes Hypertrophy That Is Prevented by Taurine via β-alanine-Sensitive NaNutrients · 2021Article
- Activation of KCNQ channels located on the skeletal muscle membrane by retigabine and its influence on the maximal muscle force in rat muscle strips.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- β-Adrenergic modulation of skeletal muscle contraction: key role of excitation-contraction coupling.The Journal of physiology · 2015Review
- Apparent lack of physical or functional interaction between CaV1.1 and its distal C terminus.The Journal of general physiology · 2015Article
- Regulation of Cardiac Calcium Channels in the Fight-or-Flight Response.Current molecular pharmacology · 2015Review
- Control of neuronal voltage-gated calcium ion channels from RNA to protein.Trends in neurosciences · 2013Review
- Creating order from chaos: cellular regulation by kinase anchoring.Annual review of pharmacology and toxicology · 2013Review
- 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
- Beta-adrenergic-regulated phosphorylation of the skeletal muscle Ca(V)1.1 channel in the fight-or-flight response.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Networking with AKAPs: context-dependent regulation of anchored enzymes.Molecular interventions · 2010Review
- Review
- Embracing emerging paradigms of G protein-coupled receptor agonism and signaling to address airway smooth muscle pathobiology in asthma.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- An anchored PKA and PDE4 complex regulates subplasmalemmal cAMP dynamics.The EMBO journal · 2006Article
- Compartmentalized cAMP/PKA signalling regulates cardiac excitation-contraction coupling.Journal of muscle research and cell motility · 2006Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Skeletal muscle L-type Ca2+ channels respond to trains of brief depolarizations with a strong shift of the voltage dependence of channel activation toward more negative membrane potentials and slowing of channel deactivation. Increased Ca2+ entry resulting from this potentiation of channel activity may increase contractile force in response to tetanic stimuli. This voltage-dependent Ca2+ channel potentiation requires phosphorylation by cAMP-dependent protein kinase (PKA) at a rate that suggests that kinase and channel may be maintained in close proximity through kinase anchoring. A peptide derived from the conserved kinase-binding domain of a PKA-anchoring protein (AKAP) prevents potentiation by endogenous PKA as effectively as inhibition of PKA by a specific peptide inhibitor or by omission of ATP from the intracellular solution. In contrast, a proline-substituted mutant of AKAP peptide has no effect. Potentiation in the presence of 2 microM exogenous catalytic subunit of PKA is unaffected, indicating that kinase anchoring is specifically blocked by the AKAP peptide. No effects of these agents were observed on the level or voltage dependence of basal Ca2+ channel activity before potentiation, suggesting that close physical proximity between the skeletal muscle Ca2+ channel and PKA is critical for voltage-dependent potentiation of Ca2+ channel activity but not for basal activity.
Indexed as
Identifiers
What 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.