PTAFR Knockout Cell Line (A549)

The choice depends on whether you are studying PTAFR's role as the platelet-activating factor (PAF) receptor in lung biology or its emerging functions in lung cancer biology. The Knockout line is the standard tool for asking whether PTAFR is required for PAF-induced signaling — PAFR is a Gq/Gi-coupled GPCR mediating inflammatory and proliferative responses to PAF and structurally related oxidized phospholipids. Overexpression is useful for studying PAFR in cancer contexts. For lung biology and cancer research, the EDITGENE PTAFR Knockout in A-549 is highly relevant — A-549 is an NSCLC model, and PAFR signaling has been implicated in lung cancer progression, particularly post-chemotherapy where oxidized phospholipids from dying cells activate PAFR on surviving tumor cells. Rescue with wild-type or signaling-deficient PAFR enables structure-function studies. The knockout is a critical specificity control for PAFR antagonists (rupatadine, lexipafant) in research applications.

Primary applications: • PAF-induced signaling: intracellular calcium mobilization and ERK activation following PAF stimulation in lung cancer context. • Chemotherapy-induced tumor regrowth: studies of oxidized phospholipid-PAFR signaling in chemotherapy survivors — emerging mechanism of post-chemotherapy tumor progression. • Inflammatory response: PAF-induced inflammatory cytokine production and downstream signaling in epithelial context. • PAFR antagonist specificity: critical genetic control for rupatadine, lexipafant, and other PAFR-targeting compounds. EDITGENE recommends this model for researchers investigating platelet-activating factor receptor biology, lung cancer-associated PAF signaling, and PAFR-targeted research applications.

Yes. PAFR rescue experiments require attention to GPCR topology: • Construct design: use a codon-modified PTAFR sequence with a small intracellular C-terminal tag (FLAG, HA). PAFR is a seven-transmembrane GPCR — preserve extracellular ligand-binding regions. • Signaling-deficient rescue: DRY motif mutations enable separating ligand binding from intracellular signaling. • Functional readout: rescue should restore PAF-induced calcium mobilization (Gq-coupled signaling) and ERK activation. A-549 transduces efficiently with lentivirus and supports stable rescue line generation.