ADRB2 Knockout Cell Line (Hela)

The choice depends on whether you are studying ADRB2 (β2-adrenergic receptor, β2-AR)'s role as a prototypical Gs-coupled GPCR or modeling its functions in asthma pharmacology and emerging biased agonism research. The Knockout line is the standard tool for asking whether β2-AR is required for these processes — ADRB2 is a Gs-coupled seven-transmembrane GPCR activated by epinephrine and norepinephrine; β2-AR is highly expressed in bronchial smooth muscle (target of asthma bronchodilators), cardiac myocytes, vascular smooth muscle, immune cells, and many other tissues; β2-AR is one of the most studied GPCRs and a foundational model for GPCR structural biology (Kobilka 2012 Nobel Prize). Overexpression is useful for studying β2-AR gain-of-function effects. For asthma pharmacology and GPCR research, the EDITGENE ADRB2 Knockout in HeLa is uniquely valuable — HeLa supports systematic structure-function studies of this prototypical GPCR. Rescue with wild-type, signaling-deficient (DRY motif mutations), or β-arrestin-binding-deficient β2-AR enables comprehensive biased agonism research. The knockout is a critical specificity tool for ⭐⭐ short-acting β2-AR agonists (SABAs: ⭐ albuterol/salbutamol, levalbuterol), long-acting β2-AR agonists (LABAs: ⭐ salmeterol, formoterol, indacaterol, olodaterol, vilanterol), inverse agonists (carvedilol, propranolol), and emerging biased β2-AR ligands.

Primary applications: • β2-AR signaling: cAMP elevation (Gs-coupled), phospho-ERK, and β-arrestin recruitment following isoproterenol, albuterol, salmeterol stimulation in β2-AR-null cells. • Asthma drug specificity: critical genetic control for ⭐⭐ albuterol/salbutamol (SABA), salmeterol/formoterol (LABA), and emerging biased β2-AR ligands. • Biased agonism studies: in combination with the parallel ARRB1&ARRB2 double KO in HEK293T (also available), systematic G-protein vs β-arrestin biased β2-AR ligand pharmacology. • β2-AR structural biology: rescue with wild-type, signaling-deficient, or β-arrestin-binding-deficient variants for systematic structure-function research. EDITGENE recommends this HeLa-based model as a critical specificity control for asthma drug development and biased GPCR pharmacology research — β2-AR is the prototypical biased agonism GPCR.

Yes. β2-AR rescue experiments are gold-standard for GPCR research: • Construct design: use a codon-modified ADRB2 sequence with a small intracellular C-terminal tag (FLAG, HA) — note that C-terminal tags may affect β-arrestin recruitment; consider alternative tag placement for biased agonism research. • Surface localization validation: confirm plasma membrane β2-AR by cell surface staining before ligand binding studies. • Signaling-deficient rescue: DRY motif mutations (D131N, R132H, Y133A) disrupt Gs-coupling. • Phosphorylation-site mutant rescue: C-terminal Ser/Thr cluster mutations affect GRK-mediated phosphorylation and β-arrestin recruitment. • Constitutively active rescue: CAM (constitutively active mutation) variants for studying activated receptor states. • Functional readout: rescue should restore isoproterenol-induced cAMP elevation and β-arrestin recruitment. HeLa transduces efficiently with lentivirus and supports stable rescue line generation for systematic biased agonism research.