Cystic Fibrosis (CF) is a lethal autosomal recessive disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene which functions as a cAMP-activated and phosphorylated-regulated Cl channel. The predominant mutation in the CFTR gene is a trinucleotide deletion that results in loss of a phenylalanine at amino acids 508 (ΔF508) in the CFTR protein. This mutation accounts for ~66% of all CF alleles . CFBE41o- 6.2 WT-CFTR Human CF Bronchial Epithelial Cell line is a subclone derived from the electroporation of the parental CFBE41o- cell line with an Epstein-Barr virus (EBV)-based episomal pCEP4β vector containing the 6.2 kb full length wtCFTR cDNA and a Hygromycin B resistance gene . The 6.2kb wtCFTR cDNA contains both the 5’ and 3’ UTR sequences that are known to affect translational efficiency and mRNA stability. The parental CFBE41o- is a CF human bronchial epithelial cell line, derived from a CF patient homozygous for the ΔF508 CFTR mutation and immortalized with the origin-of-replication defective SV40 plasmid (pSVori-) . In CFBE41o- 6.2 WT-CFTR cells, the levels of vector-driven wt-CFTR mRNA were found to be significantly higher than endogenous CFTR mRNA levels in normal 16HBE14o- bronchial epithelial cell (Cat. No. SCC150). However, cAMP-dependent Cl currents generated in CFBE41o- 6.2 WT-CFTR cells were not as high as those observed in 16HBE14o- cells, which express endogenous CFTR. Established CF bronchial epithelial cell lines that are complemented with either wild-type or ΔF508CFTR mRNA would help provide insights into the relationship between transgene-derived CFTR mRNA expression and rescue of cAMP-dependent Cl transport function.，官网链接：https://www.sigmaaldrich.cn/product/mm/scc160 默克 科研、开发、生产。 作为生命科学行业的全球领先供应商，我们致力于为科研、生物技术开发和生产，以及制药药物疗法开发和生产提供各类解决方案和服务。

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