ArticleBiophysical journal2010
Phospholemman modulates the gating of cardiac L-type calcium channels.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Intracellular ion accumulation in the genesis of complex action potential dynamics under cardiac diseases.Physical review. E · 2024Article
- Development of a high-affinity peptide that prevents phospholemman (PLM) inhibition of the sodium/calcium exchanger 1 (NCX1).The Biochemical journal · 2016Article
- Regulation of L-type calcium channel by phospholemman in cardiac myocytes.Journal of molecular and cellular cardiology · 2015Article
- Impact of phosphomimetic and non-phosphorylatable mutations of phospholemman on L-type calcium channels gating in HEK 293T cells.Journal of cellular and molecular medicine · 2015Article
- Structure of the Na,K-ATPase regulatory protein FXYD2b in micelles: implications for membrane-water interfacial arginines.Biochimica et biophysica acta · 2015Article
- Substrate recognition by the cell surface palmitoyl transferase DHHC5.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion.American journal of physiology. Heart and circulatory physiology · 2014Article
- L-type CaWiley interdisciplinary reviews. Membrane transport and signaling · 2014Article
- Nitric oxide regulates cardiac intracellular Na⁺ and Ca²⁺ by modulating Na/K ATPase via PKCε and phospholemman-dependent mechanism.Journal of molecular and cellular cardiology · 2013Article
- Regulation of the cardiac sodium pump.Cellular and molecular life sciences : CMLS · 2013Review
- Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.Journal of cardiac failure · 2013Article
- Article
- Phospholemman deficiency in postinfarct hearts: enhanced contractility but increased mortality.Clinical and translational science · 2012Article
- Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.American journal of physiology. Heart and circulatory physiology · 2012Article
- Using iPSC-derived neurons to uncover cellular phenotypes associated with Timothy syndrome.Nature medicine · 2011Article
- Residues 248-252 and 300-304 of the cardiac Na+/Ca2+ exchanger are involved in its regulation by phospholemman.American journal of physiology. Cell physiology · 2011Article
- Regulation of in vivo cardiac contractility by phospholemman: role of Na+/Ca2+ exchange.American journal of physiology. Heart and circulatory physiology · 2011Article
- Amino acid substitutions in the FXYD motif enhance phospholemman-induced modulation of cardiac L-type calcium channels.American journal of physiology. Cell physiology · 2010Article
- Phospholemman: a novel cardiac stress protein.Clinical and translational science · 2010Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Ca(2+) entry through L-type calcium channels (Ca(V)1.2) is critical in shaping the cardiac action potential and initiating cardiac contraction. Modulation of Ca(V)1.2 channel gating directly affects myocyte excitability and cardiac function. We have found that phospholemman (PLM), a member of the FXYD family and regulator of cardiac ion transport, coimmunoprecipitates with Ca(V)1.2 channels from guinea pig myocytes, which suggests PLM is an endogenous modulator. Cotransfection of PLM in HEK293 cells slowed Ca(V)1.2 current activation at voltages near the threshold for activation, slowed deactivation after long and strong depolarizing steps, enhanced the rate and magnitude of voltage-dependent inactivation (VDI), and slowed recovery from inactivation. However, Ca(2+)-dependent inactivation was not affected. Consistent with slower channel closing, PLM significantly increased Ca(2+) influx via Ca(V)1.2 channels during the repolarization phase of a human cardiac action potential waveform. Our results support PLM as an endogenous regulator of Ca(V)1.2 channel gating. The enhanced VDI induced by PLM may help protect the heart under conditions such as ischemia or tachycardia where the channels are depolarized for prolonged periods of time and could induce Ca(2+) overload. The time and voltage-dependent slowed deactivation could represent a gating shift that helps maintain Ca(2+) influx during the cardiac action potential waveform plateau phase.
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Registered trials
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