The GNG2 Knockout BEAS-2B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the human GNG2 gene has been disrupted, generating a heterogeneous loss-of-function model in the BEAS-2B human bronchial epithelial cell line. This product eliminates the need for single-cell cloning and provides a diverse repertoire of gene-disrupted cells, enabling robust functional investigations of GNG2-dependent signaling pathways mediated by G protein-coupled receptors (GPCRs).
BEAS-2B is an immortalized, non-tumorigenic cell line derived from normal human bronchial epithelium. It retains critical epithelial features, including expression of E-cadherin and cytokeratins, and recapitulates barrier function, mucociliary clearance, and innate immune responses. As a widely accepted in vitro model for respiratory diseases, BEAS-2B cells are used to study asthma, chronic obstructive pulmonary disease (COPD), and lung cancer, providing a physiologically relevant background for gene perturbation.
GNG2 encodes the gamma-2 subunit of heterotrimeric G proteins, which, following GPCR activation, dissociates into G?? and G?¦? dimers. The GNG2-containing G?¦? dimer directly modulates effectors such as adenylyl cyclase, phospholipase C-?? (PLC-??), PI3K, and MAPK cascades. In a representative pathway, GPCR ?? G protein ?? GNG2-?¦? dimer ?? PLC-?? generates IP3 and DAG, leading to calcium mobilization and PKC activation. This signaling is regulated by upstream GPCR ligands, receptor tyrosine kinases, GRKs, and RGS proteins, and GNG2 interacts with G?? subunits (GNAI, GNAQ), G?? subunits (GNB1-5), GPCRs, and RGS proteins, controlling proliferation, migration, and secretion.
In bronchial epithelial cells, GNG2-dependent GPCR signaling is integral to airway homeostasis. BEAS-2B cells utilize these pathways for maintaining epithelial barrier integrity, coordinating mucociliary clearance, and mounting innate immune defenses. Disruption of GNG2 in this model enables precise dissection of ?¦?-mediated signaling independently of G?? subunits, shedding light on mechanisms underlying airway repair, inflammatory cytokine release, and barrier dysfunction. Such insights are directly relevant to the pathobiology of asthma, COPD, and lung carcinogenesis, and may inform the development of targeted interventions.
This polyclonal knockout cell population is suitable for GPCR signal transduction studies, lung cancer progression research, and airway inflammation analysis. Representative assays include Western blot, RT-qPCR, cAMP and calcium flux measurement, scratch wound healing, Transwell migration, TEER, co-immunoprecipitation, and RNA-seq. It is also applicable to respiratory drug screening. Contact Ascent Research for more information.
