ArticleThe Journal of biological chemistry2003
Ca2+-calmodulin-dependent protein kinase II potentiates store-operated Ca2+ current.
Article in The Journal of biological chemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Minocycline protects neurons against glial cells-mediated bilirubin neurotoxicity.Brain research bulletin · 2020Article
- Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016Review
- Gravitational force modulates G2/M phase exit in mechanically unloaded myoblasts.Cell cycle (Georgetown, Tex.) · 2013Article
- Store-operated Ca2+ entry in sensory neurons: functional role and the effect of painful nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Inhibitory actions of mibefradil on steroidogenesis in mouse Leydig cells: involvement of Ca(2+) entry via the T-type Ca(2+) channel.Asian journal of andrology · 2010Article
- Physiological roles of STIM1 and Orai1 homologs and CRAC channels in the genetic model organism Caenorhabditis elegans.Cell calcium · 2007Review
- CRAC channel activity in C. elegans is mediated by Orai1 and STIM1 homologues and is essential for ovulation and fertility.The Journal of physiology · 2007Article
- Function of a STIM1 homologue in C. elegans: evidence that store-operated Ca2+ entry is not essential for oscillatory Ca2+ signaling and ER Ca2+ homeostasis.The Journal of general physiology · 2006Article
- Dual effect of calmodulin on store-operated Ca2+ -permeable cation channels in rabbit portal vein myocytes.British journal of pharmacology · 2006Article
- CaMKII inactivation by extracellular Ca(2+) depletion in dorsal root ganglion neurons.Cell calcium · 2006Article
- Group VIA phospholipase A2 forms a signaling complex with the calcium/calmodulin-dependent protein kinase IIbeta expressed in pancreatic islet beta-cells.The Journal of biological chemistry · 2005Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A rise in intracellular Ca2+ (Ca2+i) mediates various cellular functions ranging from fertilization to gene expression. A ubiquitous Ca2+ influx pathway that contributes significantly to the generation of Ca2+i signals, especially in non-excitable cells, is store-operated Ca2+ entry (SOCE). Consequently, the modulation of SOCE current affects Ca2+i dynamics and thus the ensuing cellular response. Therefore, it is important to define the mechanisms that regulate SOCE. Here we show that a rise in Ca2+i potentiates SOCE. This potentiation is mediated by Ca2+-calmodulin-dependent protein kinase II (CaMKII), because inhibition of endogenous CaMKII activity abrogates Ca2+i-mediated SOCE potentiation and expression of constitutively active CaMKII potentiates SOCE current independently of Ca2+i. Moreover, we present evidence that CaMKII potentiates SOCE by altering SOCE channel gating. The regulation of SOCE by CaMKII defines a novel modulatory mechanism of SOCE with important physiological consequences.
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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.