ArticleThe Journal of physiology2002
Cytoskeletal disrupting agents prevent calmodulin kinase, IQ domain and voltage-dependent facilitation of L-type Ca2+ channels.
Article in The Journal of physiology, 2002. 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 It has been retracted, and should not be counted.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 20 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.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Removal of the mechanoprotective influence of the cytoskeleton reveals PIEZO1 is gated by bilayer tension.Nature communications · 2016Article
- Phosphorylating Titin's Cardiac N2B Element by ERK2 or CaMKIIδ Lowers the Single Molecule and Cardiac Muscle Force.Biophysical journal · 2015Article
- A novel calmodulin site in the Cav1.2 N-terminus regulates calcium-dependent inactivation.Pflugers Archiv : European journal of physiology · 2014Article
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Competition between α-actinin and Ca²⁺-calmodulin controls surface retention of the L-type Ca²⁺ channel Ca(V)1.2.Neuron · 2013Article
- Cardiac calmodulin kinase: a potential target for drug design.Current medicinal chemistry · 2011Review
- Alterations of L-type calcium current and cardiac function in CaMKII{delta} knockout mice.Circulation research · 2010Article
- CaMKII associates with CaV1.2 L-type calcium channels via selected beta subunits to enhance regulatory phosphorylation.Journal of neurochemistry · 2010Article
- Retinoschisin, a new binding partner for L-type voltage-gated calcium channels in the retina.The Journal of biological chemistry · 2009Article
- Ca2+/calmodulin-dependent protein kinase II-dependent remodeling of Ca2+ current in pressure overload heart failure.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 inhibition targeted to the sarcoplasmic reticulum inhibits frequency-dependent acceleration of relaxation and Ca2+ current facilitation.Journal of molecular and cellular cardiology · 2007Article
- Molecular basis for the modulation of native T-type Ca2+ channels in vivo by Ca2+/calmodulin-dependent protein kinase II.The Journal of clinical investigation · 2006Article
- Calmodulin kinase II accelerates L-type Ca2+ current recovery from inactivation and compensates for the direct inhibitory effect of [Ca2+]i in rat ventricular myocytes.The Journal of physiology · 2006Article
- Modeling the actions of beta-adrenergic signaling on excitation--contraction coupling processes.Annals of the New York Academy of Sciences · 2004Article
- Targeting of calcium/calmodulin-dependent protein kinase II.The Biochemical journal · 2004Review
- Calmodulin kinase is functionally targeted to the action potential plateau for regulation of L-type Ca2+ current in rabbit cardiomyocytes.The Journal of physiology · 2004Article
- A mechanism for the direct regulation of T-type calcium channels by Ca2+/calmodulin-dependent kinase II.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- C terminus L-type Ca2+ channel calmodulin-binding domains are 'auto-agonist' ligands in rabbit ventricular myocytes.The Journal of physiology · 2003Article
- Modulation of cardiac Ca(V)1.2 channels by dihydropyridine and phosphatase inhibitor requires Ser-1142 in the domain III pore loop.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
Corrections and comments
- Retraction · 2015-05-01Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Objections by Author(s) · · Published by The Physiological Society (UK);
- Commented on by
- Erratum issued
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A calmodulin (CaM) binding 'IQ' domain on the L-type Ca(2+) channel (LTCC) C terminus and calmodulin kinase II (CaMK) both signal increases in LTCC opening probability (P(o)) by shifting LTCCs into a gating mode (mode 2) with long openings through a process called facilitation. However, the mechanism whereby CaMK and the IQ domain are targeted to LTCCs is unknown. Endogenous CaMK is targeted to LTCCs in excised cell membrane patches because LTCC P(o) increased significantly in CaM-enriched (20 microM) bath solution and this effect was prevented by a specific CaMK inhibitory peptide, but not by an inactive control peptide. Pre-exposure of myocytes to the cytoskeletal disrupting agents nocodazole (microtubule specific) or cytochalasin D (microfilament specific) prevented the effects of CaM-dependent increases in P(o) of LTCCs in excised membrane patches. Neither cytochalasin D nor nocodazole altered the distribution of LTCC gating modes under basal conditions in on-cell mode or excised cell membrane patches, but each of these agents occluded the response of LTCCs to exogenous, constitutively active CaMK and to an IQ-mimetic peptide (IQmp). Cytochalasin D and nocodazole pretreatment also prevented LTCC facilitation that followed a cell membrane depolarizing prepulse. In contrast, cytochalasin D and nocodazole did not affect the increase in LTCC P(o) or prevent the shift to mode 2 gating in response to protein kinase A, indicating that cytoskeletal disruption specifically prevents prepulse, CaMK and IQ-dependent LTCC facilitation.
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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.