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Chloride channels are a diverse group of proteins that regulate fundamental cellular processes including stabilization of cell membrane potential, transepithelial transport, maintenance of intracellular pH, and regulation of cell volume. De plus, nous expédions CLIC4 Protéines (20) et CLIC4 Kits (8) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal CLIC4 Primary Antibody pour ICC, IF - ABIN4299203
Lomnytska, Becker, Gemoll, Lundgren, Habermann, Olsson, Bodin, Engström, Hellman, Hellman, Hellström, Andersson, Mints, Auer: Impact of genomic stability on protein expression in endometrioid endometrial cancer. dans British journal of cancer 2012
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Human Polyclonal CLIC4 Primary Antibody pour ELISA, ICC - ABIN314274
Suh, Crutchley, Koochek, Ryscavage, Bhat, Tanaka, Oshima, Fitzgerald, Yuspa: Reciprocal modifications of CLIC4 in tumor epithelium and stroma mark malignant progression of multiple human cancers. dans Clinical cancer research : an official journal of the American Association for Cancer Research 2007
CLIC4 and Ihh (Montrer IHH Anticorps) could serve as biological markers for the progression, metastasis and/or invasiveness of pancreatic ductal adenocarcinoma.
in malignant pleural mesothelioma, the gene expressions of CLIC3 (Montrer CLIC3 Anticorps) and CLIC4 were significantly increased compared to controls
CLIC1 (Montrer CLIC1 Anticorps) and CLIC4 are overexpressed in specific tumor types or their corresponding stroma and change localization and function from hydrophilic cytosolic to integral transmembrane proteins. (Review)
CLIC4 knockdown decreases cell-matrix adhesion, cell spreading and integrin signaling, whereas it increases cell motility.
CLIC4, ERp29 (Montrer ERP29 Anticorps), and Smac/DIABLO (Montrer DIABLO Anticorps) integrated into a novel panel based on cancer stem-like cells in association with metastasis stratify the prognostic risks of colorectal cancer.
This study investigated the proteome modulated by oncogenic KRAS in immortalized airway epithelial cells.
Increased CLIC4 expression is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension.
CLIC4 increases tumor cell migration and invasion in a TGF-beta (Montrer TGFB1 Anticorps)-dependent manner.
In addition to CLIC1 (Montrer CLIC1 Anticorps) and TPM1 (Montrer TPM1 Anticorps), which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2 (Montrer TPM2 Anticorps), TPM3 (Montrer TPM3 Anticorps), and TPM4 (Montrer TPM4 Anticorps) were present in ovarian cancer patient sera at significantly elevated levels compared with controls.
Our data indicate that CLIC4 protein may be a key element in the apoptotic response to oxidative stress.
Results indicate CLICs (CLIC1 (Montrer CLIC1 Anticorps), CLIC4 and CLIC5 (Montrer CLIC5 Anticorps))-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (Montrer NLRP3 Anticorps) activation.
Data, including data from studies in primary cells from knockout mice, suggest Clic1 (Montrer CLIC1 Anticorps) and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 (Montrer NLRP3 Anticorps) inflammasomes; in LPS (Montrer TLR4 Anticorps) macrophage activation, Clic1 (Montrer CLIC1 Anticorps) and Clic4 are translocated to nucleus/cell membranes. (Clic1 (Montrer CLIC1 Anticorps) = chloride intracellular channel 1 (Montrer CLIC1 Anticorps); Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 (Montrer NLRP3 Anticorps) = NLR family pyrin domain containing 3 (Montrer NLRP3 Anticorps))
study reports an alternately-spliced form of Smad7 (Montrer SMAD7 Anticorps), Smad7Delta, that is induced by TGF-beta (Montrer TGFB1 Anticorps) and CLIC4, is a dominant inhibitor of Smad7 (Montrer SMAD7 Anticorps) and enhances TGF-beta (Montrer TGFB1 Anticorps) signaling
The findings indicate that CLIC4/CLIC5A-mediated ERM (Montrer ETV5 Anticorps) activation is required for maintenance of the glomerular capillary architecture.
CLIC4 is not required for collaterogenesis but is essential for perinatal maturation of nascent collaterals through a mechanism that supports VEGF (Montrer VEGFA Anticorps) signaling.
However, the absence of CLIC4 has no significant impact on the extent of functional recovery or fibrosis following acute injury.
Data suggest that compartmentalized expression of chloride intracellular channel 4 (CLIC4) in specific adult tissues and cells provides a focus to explore potential functions of this protein.
These results indicate that CLIC4 participates in skin healing and corneal wound reepithelialization through enhancement of epithelial migration by a mechanism that may involve a compromised TGF-beta (Montrer TGFB1 Anticorps) pathway.
Data suggest that iNOS (Montrer NOS2 Anticorps)-induced nuclear CLIC4 is an essential part of the macrophage deactivation program.
Chloride channels are a diverse group of proteins that regulate fundamental cellular processes including stabilization of cell membrane potential, transepithelial transport, maintenance of intracellular pH, and regulation of cell volume. Chloride intracellular channel 4 (CLIC4) protein, encoded by the CLIC4 gene, is a member of the p64 family\; the gene is expressed in many tissues and exhibits a intracellular vesicular pattern in Panc-1 cells (pancreatic cancer cells).
chloride intracellular channel 4 like
, chloride intracellular channel protein 4
, intracellular chloride ion channel protein p64H1
, chloride intracellular channel 4 (mitochondrial)
, mitochondrial chloride intracellular channel 4
, chloride intracellular channel 4
, Chloride intracellular channel protein 4