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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.
Results show that DNA methylation (zeige HELLS ELISA Kits) 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 (zeige MMP2 ELISA Kits) activation through claudin-1 (zeige CLDN7 ELISA Kits) membrane expression
Data show that claudin-6 (CLDN6) R209Q and occludin (OCLN (zeige OCLN ELISA Kits)) P24A mutations do not affect HCV pseudoparticles (HCVpp) entry.
The expression of ASK1 (zeige MAP3K5 ELISA Kits) 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 (zeige CLDN9 ELISA Kits) can serve as entry factors in cell lines, hepatitis C virus infection into human hepatocytes is not dependent on claudin-6 and claudin-9 (zeige CLDN9 ELISA Kits).
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 (zeige INVS ELISA Kits)-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 (zeige GAL ELISA Kits) penetration assays.
the normally robust injury response mechanism of the epidermis is lost in the aging Involucrin (zeige IVL ELISA Kits)-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
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