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CLCN3 encodes a member of the voltage-gated chloride channel (ClC) family. Zusätzlich bieten wir Ihnen Chloride Channel 3 Antikörper (106) und Chloride Channel 3 Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
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ClC-3 is a potential target of 17beta-estradiol and is modulated by the ERalpha (zeige ESR1 ELISA Kits) in breast cancer cells.
SDPR (zeige SDPR ELISA Kits) variants were not associated with major depressive disorder.
Overall, these data suggest that Cavin-2 represents a useful marker for discriminating the degree of differentiation in LPS tumors.
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
Data found that CVN2 expression was signi fi cantly down-regulated in oral squamous cell carcinoma (OSCC) in vitro and in vivo and that CVN2 overexpression led to decreased proliferative activities through the CVN2/caveolin-1 (zeige CAV1 ELISA Kits)/ERK (zeige EPHB2 ELISA Kits) path- way. Furthermore, high tumoral progression occurred in CVN2-negative patients with OSCC.
Hepatocellular carcinoma patients with lower cavin-2 (zeige SDPR ELISA Kits) expression have a relatively poor prognosis.
ClC-3 promotes endometriotic cell migration and invasion.
identification of a novel metastasis suppressor gene, serum deprivation response (SDPR (zeige SDPR ELISA Kits)), localized to 2q32-33, a region reported to be associated with significant loss of heterozygosity in breast cancer, is reported.
Cavin-1 (zeige PTRF ELISA Kits) and cavin-2 (zeige SDPR ELISA Kits) are strongly expressed within caveolae-like structures within liver sinusoidal endothelial cells of the hepatitis C-related cirrhotic liver and cavin-1 (zeige PTRF ELISA Kits) would play a critical role in regulating aspects of caveolin-1 (zeige CAV1 ELISA Kits).
these results demonstrated that ClC-3 is involved in the proliferation and migration of osteosarcoma cell
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 (zeige 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 (zeige 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 (zeige CLCA1 ELISA Kits) in VSMCs function
roles of AQP-3 (zeige AQP3 ELISA Kits) in AQP-3 (zeige 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.
Our findings demonstrated that ClC-3 deficiency inhibits atherosclerotic lesion development, possibly via suppression of JNK (zeige MAPK8 ELISA Kits)/p38 MAPK (zeige MAPK14 ELISA Kits) dependent SR-A (zeige MSR1 ELISA Kits) expression and foam cell formation.
ClC-3 is specialized in mainly performing incomplete capacitive nontransporting cycles in intracellular membranes.
A local enhancement of CIC (zeige 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 calcium-independent phospholipid-binding protein whose expression increases in serum-starved cells. This protein is a substrate for protein kinase C (PKC) phosphorylation and recruits polymerase I and transcript release factor (PTRF) to caveolae. Removal of this protein causes caveolae loss and its over-expression results in caveolae deformation and membrane tubulation.
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
, phosphatidylserine binding protein
, phosphatidylserine-binding protein
, serum deprivation-response protein
, putative chloride channel ClC-3