ArticlePflugers Archiv : European journal of physiology2009
Complex modulation of L-type Ca(2+) current inactivation by sorcin in isolated rabbit cardiomyocytes.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 36 citations in OpenAlex.
- Magnesium Attenuates the Association Between Mixed Element Exposure and Depressive Symptoms in Older Adults.Toxics · 2026Article
- Sorcin regulates alveolarization and airway tissue remodeling during lung morphogenesis.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Sorcin is an early marker of neurodegeneration, CaCell death & disease · 2020Article
- Roles of Sorcin in Drug Resistance in Cancer: One Protein, Many Mechanisms, for a Novel Potential Anticancer Drug Target.Cancers · 2020Review
- Sorcin a Potential Molecular Target for Cancer Therapy.Translational oncology · 2018Review
- Sorcin ablation plus β-adrenergic stimulation generate an arrhythmogenic substrate in mouse ventricular myocytes.Journal of molecular and cellular cardiology · 2018Article
- Structural basis of Sorcin-mediated calcium-dependent signal transduction.Scientific reports · 2015Article
- Sorcin, a calcium binding protein involved in the multidrug resistance mechanisms in cancer cells.Molecules (Basel, Switzerland) · 2014Review
- The evidence of HeLa cell apoptosis induced with tetraethylammonium using proteomics and various analytical methods.The Journal of biological chemistry · 2014Article
- Article
- Sorcin links calcium signaling to vesicle trafficking, regulates Polo-like kinase 1 and is necessary for mitosis.PloS one · 2014Article
- Competitive and non-competitive regulation of calcium-dependent inactivation in CaV1.2 L-type Ca2+ channels by calmodulin and Ca2+-binding protein 1.The Journal of biological chemistry · 2013Article
- Sorcin, a potential therapeutic target for reversing multidrug resistance in cancer.Journal of physiology and biochemistry · 2012Review
- CaBP1 regulates voltage-dependent inactivation and activation of Ca(V)1.2 (L-type) calcium channels.The Journal of biological chemistry · 2011Article
- Proteomics analysis of MPP+-induced apoptosis in SH-SY5Y cells.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2011Article
- Activation of the cardiac Na(+)-Ca(2+) exchanger by sorcin via the interaction of the respective Ca(2+)-binding domains.Journal of molecular and cellular cardiology · 2010Article
- Role of ryanodine receptor subtypes in initiation and formation of calcium sparks in arterial smooth muscle: comparison with striated muscle.Journal of biomedicine & biotechnology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Modulation of the L-type Ca(2+) channel (LTCC) by sorcin was investigated by measuring the L-type Ca(2+) current (I (Ca,L)) in isolated rabbit ventricular myocytes using ruptured patch, single electrode voltage clamp in the absence of extracellular Na(+). Fifty millimolars EGTA (170 nM Ca(2+)) in the pipette solution buffered bulk cytoplasmic [Ca(2+)], but retained rapid Ca(2+)-dependant inactivation of I (Ca,L,). Recombinant sorcin (3 microM) in the pipette significantly slowed time-dependant inactivation (tau (fast): 8.8 +/- 0.9 vs. 15.1 +/- 1.7 ms). Sorcin had no significant effect on I (Ca,L,) after inhibition of the sarcoplasmic reticulum (SR). Using 10 mM 1,2-bis(o-N,N,N',N'-tetraacetic acid (170 nM Ca(2+)), I (Ca,L) inactivation was then determined by a Ca(2+) -independent, voltage-dependant process. Under these conditions, 3 microM sorcin speeded up inactivation. A similar effect was observed by substitution of Ca(2+) with Ba(2+). Down-regulation of endogenous sorcin to 27 +/- 7% using an RNAi adenoviral vector slowed inactivation of I (Ca,L) by approximately 42%. The effects of sorcin on voltage-dependant inactivation were mimicked by a truncated form of the protein containing only the Ca(2+)-binding domain. This data is consistent with two independent actions of sorcin on the LTCC: (1) slowing Ca(2+)-dependant inactivation and (2) stimulating voltage-dependant inactivation. The net effect of sorcin on the time-dependent inactivation of I (Ca,L) was a balance between these two effects. Under normal conditions, sorcin slows I (Ca,L) inactivation because the effects of Ca(2+)-dependant inactivation out-weigh the effects on voltage-dependant inactivation.
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