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- 4.7 ΔF508-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 4.7 kb ΔF508 CFTR open reading frame (ORF) cDNA and a Hygromycin B resistance gene . The 4.7 kb ΔF508 CFTR cDNA contains the trinucleotide TTT deletion at the ΔF508 locus rather than the naturally occurring CTT and thus makes it possible to differentiate between endogenous ΔF508 CFTR and plasmid derived ΔF508CFTR expression. 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-) . Established CF bronchial epithelial cell lines that are complemented with either wild-type or ΔF508CFTR mRNA will 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/scc159 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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