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CLCN3 encodes a calcium-independent phospholipid-binding protein whose expression increases in serum-starved cells. Zusätzlich bieten wir Ihnen Chloride Channel 3 Proteine (7) und Chloride Channel 3 Kits (1) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 130 products:
Mammalian Monoclonal CLCN3 Primary Antibody für WB - ABIN1304600
Gaurav, Bewtra, Agrawal: Novel CLC3 transcript variants in blood eosinophils and increased CLC3 expression in nasal lavage and blood eosinophils of asthmatics. in Immunity, inflammation and disease 2015
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Rat (Rattus) Polyclonal CLCN3 Primary Antibody für WB - ABIN1742509
Eckenstaler, Lessmann, Brigadski: CAPS1 effects on intragranular pH and regulation of BDNF release from secretory granules in hippocampal neurons. in Journal of cell science 2016
Human Polyclonal CLCN3 Primary Antibody für IF (p), IHC (p) - ABIN1386131
Larrouture, Nelson, Robinson, Liu, Tourkova, Schlesinger, Blair: Chloride-hydrogen antiporters ClC-3 and ClC-5 drive osteoblast mineralization and regulate fine-structure bone patterning in vitro. in Physiological reports 2015
Cow (Bovine) Polyclonal CLCN3 Primary Antibody für IHC, WB - ABIN2776327
Salazar, Love, Styers, Werner, Peden, Rodriguez, Gearing, Wainer, Faundez: AP-3-dependent mechanisms control the targeting of a chloride channel (ClC-3) in neuronal and non-neuronal cells. in The Journal of biological chemistry 2004
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we demonstrated that ClC-3 can arrest the cell cycle at the G1 phase to inhibit cell proliferation, suggesting that ClC-3 has the potential to be a novel target for hepatocellular carcinoma (HCC (zeige FAM126A Antikörper)) therapy and potentially improve the prognosis of HCC (zeige FAM126A Antikörper) patients
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 (zeige CCND1 Antikörper), cyclin dependent kinase 4 (zeige CDK4 Antikörper) and 6, and increased the expression of cyclin dependent kinase (zeige CDK1 Antikörper) inhibitors (CDKIs), p21 (zeige CDKN1A Antikörper) and p27 (zeige PAK2 Antikörper). Pretreatments of cells with p21 (zeige CDKN1A Antikörper) and p27 (zeige PAK2 Antikörper) siRNAs depleted the inhibitory effects of ClC-3 siRNA on the expression of CDK4 (zeige CDK4 Antikörper) and CDK6 (zeige CDK6 Antikörper), but not on that of cyclin D1 (zeige CCND1 Antikörper)
ClC-3 is a potential target of 17beta-estradiol and is modulated by the ERalpha (zeige ESR1 Antikörper) 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]
intracellular Cl(-) regulation by ANO1 (zeige ANO1 Antikörper)/ClC-3 participates in HER2 (zeige ERBB2 Antikörper) transcription, mediating the PI3K/AKT (zeige AKT1 Antikörper)/mTOR (zeige FRAP1 Antikörper) and/or STAT3 (zeige STAT3 Antikörper) signaling pathway(s) in HER2 (zeige ERBB2 Antikörper)-positive breast cancer cells.
Abrogating ClC-3 blunts lipopolysaccharide-induced Inflammation via blocking the TLR4 (zeige TLR4 Antikörper)/NF-kappaB (zeige NFKB1 Antikörper) 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 (zeige PTH Antikörper) 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 Antikörper) 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 Antikörper) in VSMCs function
roles of AQP-3 (zeige AQP3 Antikörper) in AQP-3 (zeige AQP3 Antikörper) 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
ClC-3 is specialized in mainly performing incomplete capacitive nontransporting cycles in intracellular membranes.
A local enhancement of CIC (zeige CIC Antikörper)-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