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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. Zusätzlich bieten wir Ihnen CLIC4 Proteine (20) und CLIC4 Kits (8) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal CLIC4 Primary Antibody für 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 für 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 (zeige IHH Antikörper) 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 (zeige CLIC3 Antikörper) and CLIC4 were significantly increased compared to controls
CLIC1 (zeige CLIC1 Antikörper) 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 (zeige ERP29 Antikörper), and Smac/DIABLO (zeige DIABLO Antikörper) 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 (zeige TGFB1 Antikörper)-dependent manner.
In addition to CLIC1 (zeige CLIC1 Antikörper) and TPM1 (zeige TPM1 Antikörper), which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2 (zeige TPM2 Antikörper), TPM3 (zeige TPM3 Antikörper), and TPM4 (zeige TPM4 Antikörper) 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 (zeige CLIC1 Antikörper), CLIC4 and CLIC5 (zeige CLIC5 Antikörper))-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (zeige NLRP3 Antikörper) activation.
Data, including data from studies in primary cells from knockout mice, suggest Clic1 (zeige CLIC1 Antikörper) and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 (zeige NLRP3 Antikörper) inflammasomes; in LPS (zeige TLR4 Antikörper) macrophage activation, Clic1 (zeige CLIC1 Antikörper) and Clic4 are translocated to nucleus/cell membranes. (Clic1 (zeige CLIC1 Antikörper) = chloride intracellular channel 1 (zeige CLIC1 Antikörper); Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 (zeige NLRP3 Antikörper) = NLR family pyrin domain containing 3 (zeige NLRP3 Antikörper))
study reports an alternately-spliced form of Smad7 (zeige SMAD7 Antikörper), Smad7Delta, that is induced by TGF-beta (zeige TGFB1 Antikörper) and CLIC4, is a dominant inhibitor of Smad7 (zeige SMAD7 Antikörper) and enhances TGF-beta (zeige TGFB1 Antikörper) signaling
The findings indicate that CLIC4/CLIC5A-mediated ERM (zeige ETV5 Antikörper) 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 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 (zeige TGFB1 Antikörper) pathway.
Data suggest that iNOS (zeige NOS2 Antikörper)-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
, Chloride intracellular channel protein 4
, chloride intracellular channel protein 4
, chloride intracellular channel 4 like
, intracellular chloride ion channel protein p64H1
, chloride intracellular channel 4 (mitochondrial)
, mitochondrial chloride intracellular channel 4