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the membrane level of claudin6 (CLDN6), a tetraspan transmembrane tight junction protein, was dramatically reduced in EphA7 translation blocking morpholino-injected embryos, but not when a splicing morpholino was used, which blocks only the full length EphA7
claudin-6 is expressed in the developing pronephric tubule and duct but not glomus. Knockdown of claudin-6 by specific morpholino led to severe defects in pronephros tubular morphogenesis and blocked the terminal differentiation of the tubule cells.
Antibodies recognizing native CLDN6 as displayed on cell surfaces and mediating complement-dependent cytotoxicity were elicited in vaccinated animals. The data suggest applications of CLDN6 displaying Virus-like particles in cancer immunotherapy.
these results suggest that Helicobacter pylori lipopolysaccharide induces TLR2 expression in the gastric adenocarcinoma cells, and that the longer the exposure to lipopolysaccharide, the greater the expression of TLR2 in the cell membrane; consequently the expression of claudin-4, -6, -7 and -9 also increases
Study provides evidence that high expression of CLDN6 confers chemoresistance on breast cancer which is mediated by GSTP1, the activity of which is regulated by p53.
CLDN6 enhances the chemoresistance to ADM via activating the AF-6/ERK signaling pathway and up-regulating cancer stem cell characters in MDAMB231 cells.
we demonstrated that the downregulation of CLDN6 is regulated through promoter methylation by DNMT1, which depends on the SMAD2 pathway, and that CLDN6 is a key regulator in the SMAD2/DNMT1/CLDN6 pathway to inhibit EMT, migration and invasion of breast cancer cells
In conclusion, this information from bioinformatics analysis will help future attempts to better understand CLDN6 regulation and functions.
high expression of CLDN 6 was observed in approx. 65% of the myxofibrosarcomas, whereas the benign soft tissue tumors did not show a high expression of CLDN 6. The expression of CLDN 6 in the myxofibrosarcomas was significantly higher than those of other tumor specimens. Among the myxofibrosarcomas, the high expression of CLDN 6 was correlated with high FNCLCC grades and high AJCC stages.
Results show that DNA methylation down-regulates CLDN6 expression through MeCP2 binding to the CLDN6 promoter, deacetylating H3 and H4, and altering chromatin structure, consequently promoting migratory and invasive phenotype in breast cancer cells.
Cldn6 was decreased in alveolar type II-like epithelial cells (A549) and primary small airway epithelial cells when exposed to cigarette smoke ext
suggest that claudin-6 induces MMP-2 activation through claudin-1 membrane expression
Data show that claudin-6 (CLDN6) R209Q and occludin (OCLN) P24A mutations do not affect HCV pseudoparticles (HCVpp) entry.
The expression of ASK1 is correlated with the level of claudin-6 in cervical carcinoma cells and tissues.
High levels of CLDN6 are associated with non-small-cell lung cancer.
The expression of claudin-6 was down regulated in gastric cancer tissue.
Only some hepatitis C virus strains efficiently use CLDN6 for infection.
This work provides a proof of concept for the use of Claudin-6 to eliminate residual undifferentiated human pluripotent stem cells from culture.
Although claudin-6 and claudin-9 can serve as entry factors in cell lines, hepatitis C virus infection into human hepatocytes is not dependent on claudin-6 and claudin-9.
ASK1 signal may play a positive role in the inhibitory effect of claudin-6 in breast cancer.
Our results show that claudin-6 protein is significantly down-regulated in breast invasive ductal carcinomas
CLDN6 is not a specific biomarker for atypical teratoid rhabdoid tumors as it is expressed in a variety of other pediatric CNS and soft tissue tumors.
When pregnant dams were further exposed to secondhand smoke, Claudin-6 mRNA expression in embryos decreased through gestation and into post-natal periods.
Cldn6 was markedly decreased in the lungs of mice exposed to acute tobacco sm
These data reveal captivating information suggesting a role for Cldn6 in lungs exposed to tobacco smoke and suggest that further research is necessary in order to fully explain roles for tight junctional components such as Cldn6
Over-expression of Claudin 6 during embryogenesis delays lung morphogenesis.
Cldn6 is expressed by pulmonary epithelium during lung organogenesis.
The Inv-Cldn6-CDelta206 transgenic mice displayed a developmental delay in epidermal permeability barrier formation, as shown by the expression of keratins and Cldns, and by X-Gal penetration assays.
the normally robust injury response mechanism of the epidermis is lost in the aging Involucrin-Cldn6-CDelta196 transgenic epidermis
Permeability barrier dysfunction in transgenic mice overexpressing claudin 6.
Cldn6 plays a role in the differentiation processes of the epidermis and hair follicle
Claudin-6 mRNA was found to be differentially expressed in four different adipose tissues, and up-regulated in each fat depot of mice fed a high-fat diet. Levels of claudin-6 transcripts were increased during differentiation of 3T3-L1 ce
developmentally expressed claudin isoforms include claudin 6, claudin 9, and claudin 13
Results demonstrate that the overexpression of a tail truncation mutant of claudin 6 (Cldn6) mislocalizes Cldn6 and other Cldn proteins to the cytoplasm and triggers a postnatal increase in proliferation and aberrant differentiation of the epidermis.
Tight junctions containing claudin 6 are essential for blastocyst formation in preimplantation mouse embryos
Expression analysis in mice has shown that Claudin-6 is one of the few genes that allows for the targeting of the definitive endoderm throughout the entire anterior-posterior axis, before and after gut tube patterning.
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. This gene encodes a component of tight junction strands, which is a member of the claudin family. The protein is an integral membrane protein and is one of the entry cofactors for hepatitis C virus. The gene methylation may be involved in esophageal tumorigenesis. This gene is adjacent to another family member CLDN9 on chromosome 16.
, tight junction molecule claudin 6