ArticleThe Journal of physiology2004
Identification of an N-terminal amino acid of the CLC-3 chloride channel critical in phosphorylation-dependent activation of a CaMKII-activated chloride current.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- Chloride/proton antiporters ClC3 and ClC5 support bone formation in mice.Bone reports · 2024Article
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Cellular and extracellular matrix of bone, with principles of synthesis and dependency of mineral deposition on cell membrane transport.American journal of physiology. Cell physiology · 2020Review
- The signaling role for chloride in the bidirectional communication between neurons and astrocytes.Neuroscience letters · 2019Review
- Identification of Chloride Channels CLCN3 and CLCN5 Mediating the Excitatory ClFrontiers in molecular neuroscience · 2018Article
- CaMKII-mediated phosphorylation of GluN2B regulates recombinant NMDA receptor currents in a chloride-dependent manner.Molecular and cellular neurosciences · 2017Article
- Threonine532 phosphorylation in ClC-3 channels is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells.British journal of pharmacology · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Depolarization-induced depression of inhibitory transmission in cerebellar Purkinje cells.Physiological reports · 2013Article
- The ClC-3 chloride channel and osmoregulation in the European sea bass, Dicentrarchus labrax.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2013Article
- Regulatory phosphorylation induces extracellular conformational changes in a CLC anion channel.Biophysical journal · 2013Article
- Calcium entry via TRPC1 channels activates chloride currents in human glioma cells.Cell calcium · 2013Article
- CLC-3 chloride channels moderate long-term potentiation at Schaffer collateral-CA1 synapses.The Journal of physiology · 2013Article
- Functional regulation of ClC-3 in the migration of vascular smooth muscle cells.Hypertension (Dallas, Tex. : 1979) · 2013Article
- CLC anion channel regulatory phosphorylation and conserved signal transduction domains.Biophysical journal · 2012Article
- CaMKII inhibition hyperpolarizes membrane and blocks nitrergic IJP by closing a Cl(-) conductance in intestinal smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Differential regulation of a CLC anion channel by SPAK kinase ortholog-mediated multisite phosphorylation.American journal of physiology. Cell physiology · 2012Article
- Kinase activation of ClC-3 accelerates cytoplasmic condensation during mitotic cell rounding.American journal of physiology. Cell physiology · 2012Article
- Activation of swelling-activated chloride current by tumor necrosis factor-alpha requires ClC-3-dependent endosomal reactive oxygen production.The Journal of biological chemistry · 2010Article
- Molecular interaction and functional regulation of ClC-3 by Ca2+/calmodulin-dependent protein kinase II (CaMKII) in human malignant glioma.The Journal of biological chemistry · 2010Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
CLC-3, a member of the CLC family of chloride channels, mediates function in many cell types in the body. The multifunctional calcium-calmodulin-dependent protein kinase II (CaMKII) has been shown to activate recombinant CLC-3 stably expressed in tsA cells, a human embryonic kidney cell line derivative, and natively expressed channel protein in a human colonic tumour cell line T84. We examined the CaMKII-dependent regulation of CLC-3 in a smooth muscle cell model as well as in the human colonic tumour cell line, HT29, using whole-cell voltage clamp. In CLC-3-expressing cells, we observed the activation of a Cl(-) conductance following intracellular introduction of the isolated autonomous CaMKII into the voltage-clamped cell via the patch pipette. The CaMKII-dependent Cl(-) conductance was not observed following exposure of the cells to 1 microm autocamtide inhibitory peptide (AIP), a selective inhibitor of CaMKII. Arterial smooth muscle cells express a robust CaMKII-activated Cl(-) conductance; however, CLC-3(-/-) cells did not. The N-terminus of CLC-3, which contains a CaMKII consensus sequence, was phosphorylated by CaMKII in vitro, and mutation of the serine at position 109 (S109A) abolished the CaMKII-dependent Cl(-) conductance, indicating that this residue is important in the gating of CLC-3 at the plasma membrane.
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