ArticleThe Journal of biological chemistry2012
Modulation of inositol 1,4,5-trisphosphate receptor type 2 channel activity by Ca2+/calmodulin-dependent protein kinase II (CaMKII)-mediated phosphorylation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Calcineurin-NFATc regulates type 2 inositol 1,4,5-trisphosphate receptor (InsP3R2) expression during cardiac remodeling.The Journal of biological chemistry · 2014Trial
- Stress-Induced calcium mishandling in cardiac (Patho)physiology.Cellular and molecular life sciences : CMLS · 2025Review
- Using CRISPR-Cas9/phosphoproteomics to identify substrates of calcium/calmodulin-dependent kinase 2δ.The Journal of biological chemistry · 2023Article
- Inositol 1,4,5-trisphosphate receptor - reactive oxygen signaling domain regulates excitation-contraction coupling in atrial myocytes.Journal of molecular and cellular cardiology · 2022Article
- Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021Review
- Research progress on the role of CaMKII in heart disease.American journal of translational research · 2020Review
- Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKIIδ expression in the aged atrium.Cardiovascular research · 2018Article
- Article
- Type 2 inositol trisphosphate receptor gene expression in hepatocytes is regulated by cyclic AMP.Biochemical and biophysical research communications · 2017Article
- Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016Review
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- Gene expression profiles of patients with cerebral hematoma following spontaneous intracerebral hemorrhage.Molecular medicine reports · 2014Article
- CaMKII regulation of cardiac ryanodine receptors and inositol triphosphate receptors.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
InsP(3)-mediated calcium release through the type 2 inositol 1,4,5-trisphosphate receptor (InsP(3)R2) in cardiac myocytes results in the activation of associated CaMKII, thus enabling the kinase to act on downstream targets, such as histone deacetylases 4 and 5 (HDAC4 and HDAC5). The CaMKII activity also feedback modulates InsP(3)R2 function by direct phosphorylation and results in a dramatic decrease in the receptor-channel open probability (P(o)). We have identified S150 in the InsP(3)R2 core suppressor domain (amino acids 1-225) as the specific residue that is phosphorylated by CaMKII. Site-directed mutagenesis reveals that S150 is the CaMKII phosphorylation site responsible for modulation of channel activity. Nonphosphorylatable (S150A) and phosphomimetic (S150E) mutations were studied in planar lipid bilayers. The InsP(3)R2 S150A channel showed no decrease in activity when treated with CaMKII. Conversely, the phosphomimetic (S150E) channel displayed a very low P(o) under normal recording conditions in the absence of CaMKII (2 μM InsP(3) and 250 nM [Ca(2+)](FREE)) and mimicked a WT channel that has been phosphorylated by CaMKII. Phopho-specific antibodies demonstrate that InsP(3)R2 Ser-150 is phosphorylated in vivo by CaMKIIδ. The results of this study show that serine 150 of the InsP(3)R2 is phosphorylated by CaMKII and results in a decrease in the channel open probability.
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Registered trials
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