ArticleMolecular cell2006
L-type Ca2+ channel facilitation mediated by phosphorylation of the beta subunit by CaMKII.
Article in Molecular cell, 2006. 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 It has been retracted, and should not be counted.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 107 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
107 citing papers in PubMed, 182 citations in OpenAlex.
- Using CRISPR-Cas9/phosphoproteomics to identify substrates of calcium/calmodulin-dependent kinase 2δ.The Journal of biological chemistry · 2023Article
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Serotonergic Modulation of Persistent Inward Currents in Serotonergic Neurons of Medulla in ePet-EYFP Mice.Frontiers in neural circuits · 2021Article
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- Wenxin Keli for the Treatment of Arrhythmia-Systems Pharmacology andFrontiers in pharmacology · 2021Article
- Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.EBioMedicine · 2020Article
- Challenges and Opportunities for Therapeutic Targeting of Calmodulin Kinase II in Heart.Frontiers in pharmacology · 2020Review
- A Mathematical Model of the Mouse Atrial Myocyte With Inter-Atrial Electrophysiological Heterogeneity.Frontiers in physiology · 2020Article
- 1,25-Dihydroxyvitamin D modulates L-type voltage-gated calcium channels in a subset of neurons in the developing mouse prefrontal cortex.Translational psychiatry · 2019Article
- Secretoneurin to the Rescue?: Maybe or Maybe Not.Circulation. Arrhythmia and electrophysiology · 2019Article
- Mitochondrial-Mediated Oxidative CaJournal of the American Heart Association · 2018Article
- Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus.Frontiers in physiology · 2018Review
- Astragalus Granule Prevents CaEvidence-based complementary and alternative medicine : eCAM · 2017Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- Abnormal alterations in the Ca²⁺/CaV1.2/calmodulin/caMKII signaling pathway in a tremor rat model and in cultured hippocampal neurons exposed to Mg²⁺-free solution.Molecular medicine reports · 2015Article
- A Polybasic Plasma Membrane Binding Motif in the I-II Linker Stabilizes Voltage-gated CaV1.2 Calcium Channel Function.The Journal of biological chemistry · 2015Article
- Role of CaMKII in cardiac arrhythmias.Trends in cardiovascular medicine · 2015Review
- The Cav1.2 N terminus contains a CaM kinase site that modulates channel trafficking and function.Pflugers Archiv : European journal of physiology · 2015Article
- CaMKII plays a part in the chondrogenesis of bone marrow-derived mesenchymal stem cells.International journal of clinical and experimental pathology · 2015Article
- Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases.Frontiers in pharmacology · 2015Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2015-04-16Falsification/Fabrication of Data · Investigation by ORI · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author ·
- Commented on by
- Commented on by
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
L-type Ca(2+) channels (LTCCs) are major entry points for Ca(2+) in many cells. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is associated with cardiac LTCC complexes and increases channel open probability (P(O)) to dynamically increase Ca(2+) current (I(Ca)) and augment cellular Ca(2+) signaling by a process called facilitation. However, the critical molecular mechanisms for CaMKII localization to LTCCs and I(Ca) facilitation in cardiomyocytes have not been defined. We show CaMKII binds to the LTCC beta(2a) subunit and preferentially phosphorylates Thr498 in beta(2a). Mutation of Thr498 to Ala (T498A) in beta(2a) prevents CaMKII-mediated increases in the P(O) of recombinant LTCCs. Moreover, expression of beta(2a)(T498A) in adult cardiomyocytes ablates CaMKII-mediated I(Ca) facilitation, demonstrating that phosphorylation of beta(2a) at Thr498 modulates native calcium channels. These findings reveal a molecular mechanism for targeting CaMKII to LTCCs and facilitating I(Ca) that may modulate Ca(2+) entry in diverse cell types coexpressing CaMKII and the beta(2a) subunit.
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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.