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- 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-) . CFBE14o- displays all ion transport properties characteristic of cystic fibrosis such as defective cAMP-dependent chloride transport and intact calcium-dependent chloride transport. Under appropriate culture conditions, CFBE41o- forms tight junctions to give a polarized epithelium . The CFBE41o- cell line has also been used to generate subclones complemented with wild-type or ΔF508CFTR that possess differing levels of transgene-derived CFTR mRNA expression . These complemented CFBE41o- subclones (Cat. No. SCC158 – SCC161) suggest a direct correlation in CFTR mRNA expression levels to the number of active CFTR channels .，官网链接：https://www.sigmaaldrich.cn/product/mm/scc151 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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