ArticleThe Journal of physiology2001
Calmodulin kinase and a calmodulin-binding 'IQ' domain facilitate L-type Ca2+ current in rabbit ventricular myocytes by a common mechanism.
Article in The Journal of physiology, 2001. 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 It has been retracted, and should not be counted.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 24 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.
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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
24 citing papers in PubMed, 53 citations in OpenAlex.
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- The Cav1.2 N terminus contains a CaM kinase site that modulates channel trafficking and function.Pflugers Archiv : European journal of physiology · 2015Article
- Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels.Current molecular pharmacology · 2015Review
- Calmodulin regulation (calmodulation) of voltage-gated calcium channels.The Journal of general physiology · 2014Review
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Localized calcineurin confers Ca2+-dependent inactivation on neuronal L-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Calcium signaling in cardiac myocytes.Cold Spring Harbor perspectives in biology · 2011Review
- Ca2+-calmodulin-dependent protein kinase II represses cardiac transcription of the L-type calcium channel alpha(1C)-subunit gene (Cacna1c) by DREAM translocation.The Journal of physiology · 2011Article
- L-type calcium channel auto-regulation of transcription.Cell calcium · 2011Review
- Cardiac calmodulin kinase: a potential target for drug design.Current medicinal chemistry · 2011Review
- Facilitation of murine cardiac L-type Ca(v)1.2 channel is modulated by calmodulin kinase II-dependent phosphorylation of S1512 and S1570.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Ca2+-dependent facilitation of Cav1.3 Ca2+ channels by densin and Ca2+/calmodulin-dependent protein kinase II.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Regulation of excitation-contraction coupling in mouse cardiac myocytes: integrative analysis with mathematical modelling.BMC physiology · 2009Article
- Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation-contraction coupling, and cardiac arrhythmias.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- CaMKII-induced shift in modal gating explains L-type Ca(2+) current facilitation: a modeling study.Biophysical journal · 2009Article
- Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes.Biophysical journal · 2008Article
- Temporal dissociation of frequency-dependent acceleration of relaxation and protein phosphorylation by CaMKII.Journal of molecular and cellular cardiology · 2007Article
- CaMKII, an emerging molecular driver for calcium homeostasis, arrhythmias, and cardiac dysfunction.Journal of molecular medicine (Berlin, Germany) · 2007Review
- 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
- 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
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); Article is Sept 2001 (vol. 535, iss. 3, no day given);
- Commented on by
- Commented on by
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
1. Ca2+-calmodulin-dependent protein kinase II (CaMK) and a calmodulin (CaM)-binding 'IQ' domain (IQ) are both implicated in Ca2+-dependent regulation of L-type Ca2+ current (I(Ca)). We used an IQ-mimetic peptide (IQmp), under conditions in which CaMK activity was controlled, to test the relationship between these CaM-activated signalling elements in the regulation of L-type Ca2+ channels (LTCCs) and I(Ca) in rabbit ventricular myocytes. 2. A specific CaMK inhibitory peptide nearly abolished I(Ca) facilitation, but the facilitation was 'rescued' by cell dialysis with IQmp. 3. IQmp significantly enhanced I(Ca) facilitation and slowed the fast component of I(Ca) inactivation, compared with an inactive control peptide. Neither effect could be elicited by a more avid CaM-binding peptide, suggesting that generalized CaM buffering did not account for the effects of IQmp. 4. I(Ca) facilitation was abolished and the fast component of inactivation eliminated by ryanodine, caffeine or thapsigargin, suggesting that the sarcoplasmic reticulum (SR) is an important source of Ca2+ for I(Ca) facilitation and inactivation. IQmp did not restore I(Ca) facilitation under these conditions. 5. Engineered Ca2+-independent CaMK and IQmp each markedly increased LTCC open probability (P(o)) in excised cell membrane patches. The LTCC P(o) increases with CaMK and IQmp were non-additive, suggesting that CaMK and IQmp are components of a shared signalling pathway. 6. Both CaMK and IQmp induced a modal gating shift in LTCCs that favoured prolonged openings, indicating that CaMK and IQmp affect LTCCs through a common biophysical mechanism. 7. These findings support the hypothesis that CaMK is required for physiological I(Ca) facilitation in cardiac myocytes. Both CaMK and IQmp were able to induce a modal gating shift in LTCCs, suggesting that each of these signalling elements is important for Ca2+-CaM-dependent LTCC facilitation in cardiac myocytes.
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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.