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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. 再加上，我们可以发CLIC4 蛋白 (20) 和 CLIC4 试剂盒 (8)和数多这个蛋白质的别的产品。
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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
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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
Human Polyclonal CLIC4 Primary Antibody for IHC (p), WB - ABIN391815
Zou, Yang, Li, Liu, Yuan: Association of chloride intracellular channel 4 and Indian hedgehog proteins with survival of patients with pancreatic ductal adenocarcinoma. in International journal of experimental pathology 2017
CLIC4 and Ihh (显示 IHH 抗体) 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 (显示 CLIC3 抗体) and CLIC4 were significantly increased compared to controls
CLIC1 (显示 CLIC1 抗体) 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 (显示 ERP29 抗体), and Smac/DIABLO (显示 DIABLO 抗体) 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 (显示 TGFB1 抗体)-dependent manner.
In addition to CLIC1 (显示 CLIC1 抗体) and TPM1 (显示 TPM1 抗体), which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2 (显示 TPM2 抗体), TPM3 (显示 TPM3 抗体), and TPM4 (显示 TPM4 抗体) 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 (显示 CLIC1 抗体), CLIC4 and CLIC5 (显示 CLIC5 抗体))-dependent chloride efflux as an essential and proximal upstream event for NLRP3 (显示 NLRP3 抗体) activation.
Data, including data from studies in primary cells from knockout mice, suggest Clic1 (显示 CLIC1 抗体) and Clic4 participate in signaling interleukin 1beta secretion and in activation of Nlrp3 (显示 NLRP3 抗体) inflammasomes; in LPS (显示 TLR4 抗体) macrophage activation, Clic1 (显示 CLIC1 抗体) and Clic4 are translocated to nucleus/cell membranes. (Clic1 (显示 CLIC1 抗体) = chloride intracellular channel 1 (显示 CLIC1 抗体); Clic4 = chloride intracellular channel 4, mitochondrial; Nlrp3 (显示 NLRP3 抗体) = NLR family pyrin domain containing 3 (显示 NLRP3 抗体))
study reports an alternately-spliced form of Smad7 (显示 SMAD7 抗体), Smad7Delta, that is induced by TGF-beta (显示 TGFB1 抗体) and CLIC4, is a dominant inhibitor of Smad7 (显示 SMAD7 抗体) and enhances TGF-beta (显示 TGFB1 抗体) signaling
The findings indicate that CLIC4/CLIC5A-mediated ERM (显示 ETV5 抗体) 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 (显示 VEGFA 抗体) 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 (显示 TGFB1 抗体) 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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