ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2005
A dynamic alpha-beta inter-subunit agonist signaling complex is a novel feedback mechanism for regulating L-type Ca2+ channel opening.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias.Reviews of physiology, biochemistry and pharmacology · 2016Review
- SR calcium handling dysfunction, stress-response signaling pathways, and atrial fibrillation.Frontiers in physiology · 2015Review
- Differential control of calcium homeostasis and vascular reactivity by Ca2+/calmodulin-dependent kinase II.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Molecular Determinants of Cav1.2 Calcium Channel Inactivation.ISRN molecular biology · 2012Review
- Single-channel monitoring of reversible L-type Ca(2+) channel Ca(V)α(1)-Ca(V)β subunit interaction.Biophysical journal · 2011Article
- Thermodynamic linkage between calmodulin domains binding calcium and contiguous sites in the C-terminal tail of Ca(V)1.2.Biophysical chemistry · 2011Article
- Oligomerization of Cavbeta subunits is an essential correlate of Ca2+ channel activity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Inactivation of L-type calcium channel modulated by HCN2 channel.American journal of physiology. Cell physiology · 2010Article
- CaMKII associates with CaV1.2 L-type calcium channels via selected beta subunits to enhance regulatory phosphorylation.Journal of neurochemistry · 2010Article
- CaMKII phosphorylates a threonine residue in the C-terminal tail of Cav1.2 Ca(2+) channel and modulates the interaction of the channel with calmodulin.The journal of physiological sciences : JPS · 2009Article
- Effect of Ca(v)beta subunits on structural organization of Ca(v)1.2 calcium channels.PloS one · 2009Article
- Supramolecular assemblies and localized regulation of voltage-gated ion channels.Physiological reviews · 2009Review
- Disruption of the IS6-AID linker affects voltage-gated calcium channel inactivation and facilitation.The Journal of general physiology · 2009Article
- Calmodulin-dependent gating of Ca(v)1.2 calcium channels in the absence of Ca(v)beta subunits.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- New Determinant for the CaVbeta2 subunit modulation of the CaV1.2 calcium channel.The Journal of biological chemistry · 2008Article
- Differential regulated interactions of calcium/calmodulin-dependent protein kinase II with isoforms of voltage-gated calcium channel beta subunits.Biochemistry · 2008Article
- CaMKII, an emerging molecular driver for calcium homeostasis, arrhythmias, and cardiac dysfunction.Journal of molecular medicine (Berlin, Germany) · 2007Review
Corrections and comments
- Retraction · 2015-03-01Falsification/Fabrication of Data · Falsification/Fabrication of Image · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Notice - Limited or No Information · Objections by Third Party ·
- Commented on by
- RetractedRetraction.2015
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L-type Ca2+ channels are macromolecular protein complexes in neurons and myocytes that open in response to cell membrane depolarization to supply Ca2+ for regulating gene transcription and vesicle secretion and triggering cell contraction. L-type Ca2+ channels include a pore-forming alpha and an auxiliary beta subunit, and alpha subunit openings are regulated by cellular Ca2+ through a mechanism involving the Ca2+-sensing protein calmodulin (CaM) and CaM binding motifs in the alpha subunit cytoplasmic C terminus. Here we show that these CaM binding motifs are "auto-agonists" that increase alpha subunit openings by binding the beta subunit. The CaM binding domains are necessary and sufficient for the alpha subunit C terminus to bind the beta subunit in vitro, and excess CaM blocks this interaction. Addition of CaM binding domains to native cardiac L-type Ca2+ channels in excised cell membrane patches increases openings, and this agonist effect is prevented by excess CaM. Recombinant LTCC openings are also increased by exogenous CaM binding domains by a mechanism requiring the beta subunit, and excess CaM blocks this effect. Thus, the bifunctional ability of the alpha subunit CaM binding motifs to competitively associate with the beta subunit or CaM provides a novel paradigm for feedback control of cellular Ca2+ entry.
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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.