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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.
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Human Polyclonal CLIC4 Primary Antibody for 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. in British journal of cancer 2012
Show all 3 Pubmed References
Human Polyclonal CLIC4 Primary Antibody for 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. in Clinical cancer research : an official journal of the American Association for Cancer Research 2007
CLIC4 and Ihh (show IHH Antibodies) 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 (show CLIC3 Antibodies) and CLIC4 were significantly increased compared to controls
CLIC1 (show CLIC1 Antibodies) 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 (show ERP29 Antibodies), and Smac/DIABLO (show DIABLO Antibodies) 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 (show TGFB1 Antibodies)-dependent manner.
In addition to CLIC1 (show CLIC1 Antibodies) and TPM1 (show TPM1 Antibodies), which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2 (show TPM2 Antibodies), TPM3 (show TPM3 Antibodies), and TPM4 (show TPM4 Antibodies) 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 demonstrate that down-regulating CLIC4 inhibit the proliferation and promotes the apoptosis of mouse liver cancer Hca-F cell.
Results indicate CLICs (CLIC1 (show CLIC1 Antibodies), CLIC4 and CLIC5 (show CLIC5 Antibodies))-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (show NLRP3 Antibodies) activation.
Data, including data from studies in primary cells from knockout mice, suggest Clic1 (show CLIC1 Antibodies) and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 (show NLRP3 Antibodies) inflammasomes; in LPS (show TLR4 Antibodies) macrophage activation, Clic1 (show CLIC1 Antibodies) and Clic4 are translocated to nucleus/cell membranes. (Clic1 (show CLIC1 Antibodies) = chloride intracellular channel 1 (show CLIC1 Antibodies); Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 (show NLRP3 Antibodies) = NLR family pyrin domain containing 3 (show NLRP3 Antibodies))
study reports an alternately-spliced form of Smad7 (show SMAD7 Antibodies), Smad7Delta, that is induced by TGF-beta (show TGFB1 Antibodies) and CLIC4, is a dominant inhibitor of Smad7 (show SMAD7 Antibodies) and enhances TGF-beta (show TGFB1 Antibodies) signaling
The findings indicate that CLIC4/CLIC5A-mediated ERM (show ETV5 Antibodies) 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 (show VEGFA Antibodies) 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 (show TGFB1 Antibodies) pathway.
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).
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, chloride intracellular channel protein 4
, intracellular chloride ion channel protein p64H1
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, mitochondrial chloride intracellular channel 4
, chloride intracellular channel 4
, Chloride intracellular channel protein 4