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Chloride channel 3

ClC-3, Clcn3
This gene encodes a member of the voltage-gated chloride channel (ClC) family. The encoded protein is present in all cell types and localized in plasma membranes and in intracellular vesicles. It is a multi-pass membrane protein which contains a ClC domain and two additional C-terminal CBS (cystathionine beta-synthase) domains. The ClC domain catalyzes the selective flow of Cl- ions across cell membranes, and the CBS domain may have a regulatory function. This protein plays a role in both acidification and transmitter loading of GABAergic synaptic vesicles, and in smooth muscle cell activation and neointima formation. This protein is required for lysophosphatidic acid (LPA)-activated Cl- current activity and fibroblast-to-myofibroblast differentiation. The protein activity is regulated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in glioma cells. Multiple alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: ACID, ClC-2, ClC-5, V1a, CAN
Papers on ClC-3
Down-Regulation of ClC-3 Expression Reduces Epidermal Stem Cell Migration by Inhibiting Volume-Activated Chloride Currents.
Cao et al., Chongqing, China. In J Membr Biol, Feb 2016
UNASSIGNED: ClC-3, a member of the ClC chloride (Cl(-)) channel family, has recently been proposed as the primary Cl(-) channel involved in cell volume regulation.
A Combined Approach Employing Chlorotoxin-Nanovectors and Low Dose Radiation to Reach Infiltrating Tumor Niches in Glioblastoma.
Matteoli et al., In Acs Nano, Feb 2016
We show here that a single whole brain x-rays irradiation, performed 20 hrs before nanoparticle injection, enhances the expression of the CTX targets, MMP-2 and ClC-3 and, through BBB permeabilization, potently increases the amount of internalized Ag-PNP-CTX even in dispersed cells, and generated an efficient anti-tumor synergistic effect able to inhibit in vivo tumor growth.
ClC-3 chloride channel functions as a mechanically sensitive channel in osteoblasts.
Duan et al., Xi'an, China. In Biochem Cell Biol, Dec 2015
Mechanical force also up-regulated the mRNA level of osteogenic markers such as alkaline phosphatase (Alp), bone sialoprotein (Bsp), and osteocalcin (Oc), which could be blocked or strengthened by Clcn3 siRNA or overexpressing, and Alp expression was more sensitive to the changes of ClC-3 level.
Threonine 532 phosphorylation in ClC-3 is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells.
Guan et al., Guangzhou, China. In Br J Pharmacol, Dec 2015
KEY RESULTS: In VSMC, AngII induced a ClC-3-dependent Cl(-) current that was abolished in ClC-3 null mice.
Chloride-hydrogen antiporters ClC-3 and ClC-5 drive osteoblast mineralization and regulate fine-structure bone patterning in vitro.
Blair et al., Pittsburgh, United States. In Physiol Rep, Nov 2015
Gene screening in mineralizing osteoblasts showed dramatic expression of chloride-proton antiporters ClC-3 and ClC-5.
CLC-3 channels in cancer (review).
Zhao et al., Changchun, China. In Oncol Rep, Feb 2015
CLC-3 is a member of the voltage-gated chloride channel superfamily and is expressed in many cancer cells.
Chloride Channels - New Targets for the Prevention of Stroke.
Guan et al., Guangzhou, China. In Curr Vasc Pharmacol, 2014
Recent studies have demonstrated that ClC-3, a member of the voltage-gated ClC Cl(-) channel family, is the molecular candidate for VRCC in VSMC.
Porosome in Cystic Fibrosis.
Jena, Detroit, United States. In Discoveries (craiova), 2014
Since CFTR is known to interact with the t-SNARE protein syntaxin-1A, and with the chloride channel CLC-3, which are also components of the porosome complex, the interactions between CFTR and the porosome complex in the mucin-secreting human airway epithelial cell line Calu-3 was hypothesized and tested.
Cl⁻ channels in smooth muscle cells.
Jaggar et al., In Pflugers Arch, 2014
Both "classic" and cGMP-dependent calcium (Ca2+)-activated (ClCa) channels and volume-sensitive Cl− channels are present, with TMEM16A/ANO1, bestrophins, and ClC-3, respectively, proposed as molecular candidates for these channels.
CLC channel function and dysfunction in health and disease.
Fahlke et al., Jülich, Germany. In Front Physiol, 2013
There are four human CLC channels, ClC-1, ClC-2, ClC-Ka, and ClC-Kb, and five CLC transporters, ClC-3 through -7.
ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.
Chen et al., Guangzhou, China. In Am J Physiol Cell Physiol, 2012
ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.
Cell biology and physiology of CLC chloride channels and transporters.
Jentsch et al., Berlin, Germany. In Compr Physiol, 2012
The mainly endosomal/lysosomal Cl(-)/H(+)-exchangers ClC-3 to ClC-7 may facilitate vesicular acidification by shunting currents of proton pumps and increase vesicular Cl(-) concentration.
Patterned expression of ion channel genes in mouse dorsal raphe nucleus determined with the Allen Mouse Brain Atlas.
Commons et al., Boston, United States. In Brain Res, 2012
This study demonistrated that Clcn3 gene expression in mouse dorsal raphe nucleus
Intermediate-conductance Ca(2+) -activated potassium and volume-sensitive chloride channels in endothelial progenitor cells from rat bone marrow mononuclear cells.
Zhou et al., Ningbo, China. In Acta Physiol (oxf), 2012
Our results demonstrated for the first time that rat bone marrow endothelial progenitor cells expressed volume-sensitive chloride currents and the corresponding gene and protein Clcn3.
Cell cycle-dependent subcellular distribution of ClC-3 in HeLa cells.
Chen et al., Guangzhou, China. In Histochem Cell Biol, 2012
results reveal a cell cycle-dependent change of the subcellular distribution of ClC-3 and strongly suggest that ClC-3 has nucleocytoplasmic shuttling dynamics that may play key regulatory roles during different stages of the cell cycle in tumor cells.
Activation of volume regulated chloride channels protects myocardium from ischemia/reperfusion damage in second-window ischemic preconditioning.
Duan et al., Reno, United States. In Cell Physiol Biochem, 2010
The targeted inactivation of CIC-3 gene prevented cardioprotective effects of second-window ischemic preconditioning (swIPC) but not early ischemic preconditioning (eIPC) suggesting that VRCCs may contribute differently to eIPC and swIPC.
The granular chloride channel ClC-3 is permissive for insulin secretion.
Nelson et al., Chicago, United States. In Cell Metab, 2009
These results demonstrate that in pancreatic beta cells, chloride channels, specifically ClC-3, are localized on insulin granules and play a role in insulin processing as well as insulin secretion through regulation of granular acidification.
Suppression of sulfonylurea- and glucose-induced insulin secretion in vitro and in vivo in mice lacking the chloride transport protein ClC-3.
Renström et al., Malmö, Sweden. In Cell Metab, 2009
Data establish the importance of granular Cl(-) fluxes in granule priming and provide direct evidence for the involvement of ClC-3 in the process.
Anion transport in heart.
Horowitz et al., Reno, United States. In Physiol Rev, 2000
I(Cl.Ca), and I( (ClC-3, CLCA1, and ClC-2, respectively) have recently been identified and are presently being evaluated.
Molecular identification of a volume-regulated chloride channel.
Horowitz et al., Reno, United States. In Nature, 1997
Here we report that functional expression in NIH/3T3 cells of a cardiac clone of another member of the ClC family, ClC-3, results in a large basally active chloride conductance, which is strongly modulated by cell volume and exhibits many properties identical to those of ICl.vol in native cells.
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