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CLCN3 encodes a calcium-independent phospholipid-binding protein whose expression increases in serum-starved cells. Additionally we are shipping Chloride Channel 3 Antibodies (130) and Chloride Channel 3 Proteins (7) and many more products for this protein.
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CLC-3 may get involved in proliferation, invasion, and migration of ovarian cancer cells and thus may be a useful therapeutic target.
Transfection of cells with ClC-3 siRNA decreased the expression of cyclin D1 (show CCND1 ELISA Kits), cyclin dependent kinase 4 (show CDK4 ELISA Kits) and 6, and increased the expression of cyclin dependent kinase (show CDK1 ELISA Kits) inhibitors (CDKIs), p21 (show CDKN1A ELISA Kits) and p27 (show PAK2 ELISA Kits). Pretreatments of cells with p21 (show CDKN1A ELISA Kits) and p27 (show PAK2 ELISA Kits) siRNAs depleted the inhibitory effects of ClC-3 siRNA on the expression of CDK4 (show CDK4 ELISA Kits) and CDK6 (show CDK6 ELISA Kits), but not on that of cyclin D1 (show CCND1 ELISA Kits)
ClC-3 is a potential target of 17beta-estradiol and is modulated by the ERalpha (show ESR1 ELISA Kits) in breast cancer cells.
Study provided novel and compelling evidence for the functional role of the unique CLC-3, which are significantly upregulated during ischemia, in the protection of the heart under stress
ClC-3 promotes endometriotic cell migration and invasion.
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
Abrogating ClC-3 blunts lipopolysaccharide-induced Inflammation via blocking the TLR4 (show TLR4 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) pathway.
Results have shown that the expression of ClC-3 was reduced in hypertrophic H9c2 cells, primary rat neonatal cardiomyocytes and myocardium of C57/BL/6 mice and that ClC-3 played an important role in beta-adrenergic cardiac hypertrophy.
we conclude that the expression of ClC-3 chloride channels in osteoblasts helps them respond to PTH (show PTH ELISA Kits) stimulation, which mediates osteogenic differentiation.
our findings show that Cl(-) channels can be activated by estrogen via ERa on the cell membrane and suggest that the ClC-3 Cl(-) channel may be one of the targets of estrogen in the regulation of osteoblast activity.
ClC-3 is an endogenous inhibitor of neuropathic pain development and down-regulation of ClC-3 contributes to mechanical hypersensitivity.
This study provides a new mechanism by which endophilin A2 (show SH3GL1 ELISA Kits) regulates ClC-3 channel activity, and sheds light on how ClC-3 is transported to cell membranes to play its critical role as a chloride channel (show CLCA1 ELISA Kits) in VSMCs function
roles of AQP-3 (show AQP3 ELISA Kits) in AQP-3 (show AQP3 ELISA Kits) aquaglyceroporin and ClC-3 chloride channels complex
ClC-3 plays a major role in hyperglycemia induced hippocampal neuronal apoptosis.
Threonine532 phosphorylation in ClC-3 channels is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells
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.
ClC-3 is specialized in mainly performing incomplete capacitive nontransporting cycles in intracellular membranes.
A local enhancement of CIC (show CIC ELISA Kits)-3 expression at the leading edge of the wounded epidermis was found to be specific to closing wounds.
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 transporter ClC-3
, protein kinase C-regulated chloride channel
, chloride channel Clc-3
, Chloride channel protein 3
, H(+)/Cl(-) exchange transporter 3-like
, putative chloride channel ClC-3