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CLCN3 encodes a member of the voltage-gated chloride channel (ClC) family. Additionally we are shipping Chloride Channel 3 Antibodies (87) and Chloride Channel 3 Kits (1) and many more products for this protein.
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Data suggest that ClC3/Clcn3 expression is up-regulated by mechanical stimulation (persistent static compression here) in osteoblastic cell line and appears to participate in mechanically sensitive osteogenesis and gene expression regulation.
Our findings demonstrated that ClC-3 deficiency inhibits atherosclerotic lesion development, possibly via suppression of JNK (show MAPK8 Proteins)/p38 MAPK (show MAPK14 Proteins) dependent SR-A (show MSR1 Proteins) expression and foam cell formation.
plasmalemmal ClC (show CLC Proteins)-3d, like ClC (show CLC Proteins)-3a, mediates Cd(2 (show CD2 Proteins)+)-sensitive outwardly rectifying anion currents and that ClC (show CLC Proteins)-3d is distinct from the molecular entities of acid- and volume-sensitive anion channels.
alternative splicing of Clcn3 results in proteins with different subcellular localizations, but leaves the transport function of the proteins unaffected
ClC-3 deficiency prevent preadipocytes against palmitate-induced apoptosis via suppressing ER stress, and also suggested that ClC-3 may play a role in regulating cellular apoptosis and disorders of glucose and lipid metabolism during T2DM.
Hypotonic stress can induce endocytosis in bone marrow derived macrophages and ClC-3 plays a central role in the endocytic process.
Integrin beta3 mediates cerebrovascular remodelling during hypertension via Src (show SRC Proteins)/ClC-3 signalling pathway.
ClC-3 deficiency attenuates cerebrovascular remodelling possibly via the suppression of MMPs/TIMP expression and TGF-beta1 (show TGFB1 Proteins)/Smad3 (show SMAD3 Proteins) signalling pathway in this hypertension.
CLC-3 confers chloride sensitivity to excitatory synapses, controls the magnitude of long-term potentiation and may provide a protective limit on Ca(2 (show CA2 Proteins)+) influx
we determined the level of Autofluorescent storage material in chloride channel 3 gene-deficient mice both in response to aging and following mild global ischemia
ClC-3 is specialized in mainly performing incomplete capacitive nontransporting cycles in intracellular membranes.
A local enhancement of CIC-3 expression at the leading edge of the wounded epidermis was found to be specific to closing wounds.
these results demonstrated that ClC-3 is involved in the proliferation and migration of osteosarcoma cell
Data indicate that cytoplasmic chloride channel-3 (ClC-3) plays an active and key role in tumor metastasis and may be a valuable prognostic biomarker and a therapeutic target to prevent tumor spread.
CLC3 is required in the activation and migration of human blood eosinophils.
Authors summarize the function of CLC-3 in cancer and discuss the mechanisms by which CLC-3 contributes to proliferation, apoptosis and drug resistance in cancer cells. [Review]
swelling-activated Cl currents and CLC-3 play a role in pulmonary artery smooth muscle cell proliferation, but CLC-3 channels do not underlie swelling in these cells
ClC-3 deficiency inhibited Ang II (show AGT Proteins)-induced EPC (show TCF21 Proteins) apoptosis via suppressing ROS (show ROS1 Proteins) generation derived from NADPH oxidase (show NOX1 Proteins).
our data suggest that the ClC-3 chloride channel (show CLCA1 Proteins) is an important target of cyclin D1 (show CCND1 Proteins). Cyclin D1 (show CCND1 Proteins) may regulate the functional activities of the chloride channel (show CLCA1 Proteins) via CDK4 (show CDK4 Proteins) and CDK6 (show CDK6 Proteins), and/or the expression of the chloride channel (show CLCA1 Proteins).
Suggest that ClC-3 suppression causes the inhibition of Akt (show AKT1 Proteins) and autophagy, which can enhance the therapeutic benefit of cisplatin in U251 cells.
K(Ca)3.1 and ClC-3 are expressed in tissue samples obtained from patients diagnosed with grade IV gliomas. Both K(Ca)3.1 and ClC-3 colocalize to the invading processes of glioma cells
Data indicate in umbilical vein endothelial cells transfected with ClC-3 siRNA showed activation of NF-kappaB (show NFKB1 Proteins).
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.
H(+)/Cl(-) exchange transporter 3
, chloride channel 3
, chloride channel protein 3
, Chloride channel protein 3
, chloride transporter ClC-3
, H(+)/Cl(-) exchange transporter 3-like
, chloride channel Clc-3
, putative chloride channel ClC-3
, protein kinase C-regulated chloride channel