General descriptionCystic 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 .
ApplicationCFBE41o- human CF bronchial epithelial cell line was derived from a cystic fibrosis patient homozygous for the ΔF508 CFTR mutation.
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Biochem/physiol ActionsEpithelial Cells
Preparation NoteStore in liquid nitrogen. The cells can be cultured for at least 10 passages after initial thawing without significantly affecting the cell marker expression and functionality.
Analysis Note• Each vial contains ≥ 1X10⁶ viable cells.
• Cells are tested by PCR and are negative for HPV-16, HPV-18, Hepatitis A, C, and HIV-1 & 2 viruses as assessed by a Human Essential CLEAR panel by Charles River Animal Diagnostic Services.
• Cells are negative for mycoplasma contamination.
• Each lot of cells is genotyped by STR analysis to verify the unique identity of the cell line.
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