In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The CFTR Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout of the CFTR gene in BEAS-2B human bronchial epithelial cells. CFTR functions as a cAMP-activated chloride channel regulated by PKA phosphorylation and scaffold protein NHERF1, mediating ion and fluid transport across epithelial surfaces. Loss of CFTR in this cell line abolishes cAMP-stimulated chloride secretion, disrupting airway surface liquid homeostasis and mucociliary clearance??hallmarks of cystic fibrosis. The model supports ion transport assays, CFTR modulator screening, and host-pathogen interaction studies in a differentiated airway epithelial background.
COMMD4 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17946
PDIA4 Knockout HT29 Polyclonal Cells
Cat. No. ARG14261
LRRC57 Knockout HT29 Polyclonal Cells
Cat. No. ARG13980
MTMR4 Knockout Hela Polyclonal Cells
Cat. No. ARG9013
CMBL Knockout Hela Polyclonal Cells
Cat. No. ARG8076
CMC4 Knockout AGS Polyclonal Cells
Cat. No. ARG2200
The CFTR Knockout BEAS-2B Cell Line provides a CRISPR/Cas9-mediated gene disruption of CFTR in the BEAS-2B human bronchial epithelial cell line. This knockout cell line enables loss-of-function investigation of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-activated chloride channel critical for epithelial ion and fluid transport. The CRISPR/Cas9 system was used to disrupt the CFTR locus, yielding a stable knockout that lacks functional CFTR protein, as confirmed by western blot and RT-qPCR. The model is a genetic tool for studying CFTR-dependent ion transport, cystic fibrosis pathology, and modulator pharmacology.
BEAS-2B cells are an SV40 large T-antigen immortalized normal human bronchial epithelial cell line that retains key airway epithelial characteristics, including polarized monolayer formation and mucociliary clearance functions. Widely used to model airway epithelial barrier and host defense, these cells exhibit endogenous cAMP-stimulated chloride secretion, making them physiologically relevant for CFTR studies. The immortalized background ensures consistent growth and reproducibility while maintaining differentiated features of primary bronchial cells.
CFTR is a cAMP-regulated chloride channel at the apical membrane, activated by PKA phosphorylation downstream of beta-adrenergic receptor agonists, adenosine, and forskolin. Scaffolding proteins NHERF1/EBP50 and RACK1 assemble CFTR into signaling complexes, while chaperones HSC70 and HSP90 facilitate folding and trafficking. Interactions with SNARE proteins SNAP23 and STX1A control membrane delivery. CFTR-mediated chloride secretion regulates airway surface liquid volume and inhibits the epithelial sodium channel ENaC, cooperating with anion exchangers SLC26A9 and SLC26A3 to maintain mucociliary clearance.
Knockout of CFTR in BEAS-2B cells abolishes cAMP-dependent chloride efflux, disrupting airway surface liquid homeostasis and mucociliary clearance??central defects in cystic fibrosis. This model replicates the ion transport deficiency of CF airways, enabling dissection of CFTR-dependent epithelial functions, barrier integrity, inflammatory signaling, and pathogen interactions in a reductionist in vitro system.
Typical applications include Ussing chamber measurements of transepithelial currents, chloride efflux assays, and forskolin-induced swelling in organoids for modulator screening. The cell line supports CFTR trafficking studies via cell surface biotinylation and immunofluorescence, as well as patch clamp electrophysiology. It is a valuable platform for drug discovery, host-pathogen research, and mechanistic studies of epithelial ion transport. For additional information, contact Ascent Research.
