-
High CLIC4 expression is associated with Merkel cell polyomavirus positive Merkel cell carcinoma.
-
Results provide evidence that the G4 structure formed in the CLIC4 promoter region may act as a regulatory element in regulating CLIC4 gene transcription.
-
CLIC4 and Ihh 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 and CLIC4 were significantly increased compared to controls
-
CLIC1 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, and Smac/DIABLO 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-dependent manner.
-
In addition to CLIC1 and TPM1, which were the proteins initially discovered in a xenograft mouse model, CLIC4, TPM2, TPM3, and TPM4 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.
-
These results demonstrate that CLIC4 nuclear translocation is an integral part of the cellular response to starvation.
-
Reduced CLIC4 expression and nuclear residence detected in cancer cells is associated with the altered redox state of tumor cells and the absence of detectable nuclear CLIC4 in cancers contributes to TGF-beta resistance and enhances tumor development.
-
CLIC4 may not be responsible for benign familial infantile seizures (BFIS) in a Chinese family affected with BFIS.
-
Data suggest that CLIC4 is regulated by RhoA to be targeted to the plasma membrane, where it may function not as an inducible chloride channel but rather by displaying Cys-dependent transferase activity toward a yet unknown substrate.
-
CLIC4 functions to promote endothelial cell proliferation and to regulate endothelial morphogenesis, and is thus involved in multiple steps of in vitro angiogenesis.
-
CLIC4 is differentially regulated in fibroblasts and its expression contributes to a myofibroblast phenotype
-
CLIC4 has alternate cellular functions that are distinct from their proposed roles as chloride channels
-
subcellular localization of CLIC4 in endothelial cells was dependent on whether cells were engaged in proliferation or tube formation