AXL Knockout Cell Line (A549)

The choice depends on whether you are studying AXL's role as a TAM (TYRO3-AXL-MERTK) family receptor tyrosine kinase or modeling its emerging functions as a cancer drug resistance and immunotherapy target. The Knockout line is the standard tool for asking whether AXL is required for these processes — AXL is activated by GAS6 ligand binding (also PROS1); AXL is critical for efferocytosis (apoptotic cell clearance), epithelial-mesenchymal transition (EMT), and has emerged as a major mediator of resistance to EGFR-TKIs, chemotherapy, and immunotherapy in lung and other cancers. Overexpression is useful for studying AXL gain-of-function effects. For NSCLC drug resistance research, the EDITGENE AXL Knockout in A-549 is uniquely valuable — AXL upregulation is a key mechanism of acquired resistance to osimertinib and other EGFR-TKIs in EGFR-mutated NSCLC. Rescue with wild-type or kinase-dead AXL is the standard specificity control. The knockout is a critical specificity tool for ⭐⭐ bemcentinib (BGB324, AVB-500, AXL-selective inhibitor in NSCLC and AML clinical development), enapotamab vedotin (anti-AXL ADC), TP-0903, and emerging AXL-targeted therapeutics — AXL is one of the most validated cancer drug resistance targets.

Primary applications: • GAS6-induced signaling: GAS6-stimulated phospho-AXL (Y702, Y779), phospho-AKT, phospho-ERK analysis in AXL-null NSCLC cells. • EGFR-TKI resistance: in heterologous EGFR-mutant NSCLC contexts, AXL's role in osimertinib resistance. • AXL-targeted therapy specificity: critical genetic control for ⭐⭐ bemcentinib (BGB324/AVB-500), enapotamab vedotin (anti-AXL ADC), TP-0903 in NSCLC and AML drug development. • EMT studies: epithelial-mesenchymal transition markers and migration assays given AXL's EMT-driving function. EDITGENE recommends this NSCLC model as a critical specificity control for AXL-targeted cancer therapy and TKI resistance research.

Yes. AXL rescue experiments are well-established for cancer drug resistance research: • Construct design: use a codon-modified AXL sequence with a small intracellular C-terminal tag (FLAG, HA). AXL has extracellular Ig and FN3 domains (GAS6 binding), transmembrane span, and intracellular kinase domain — preserve all elements. • Surface localization validation: confirm plasma membrane localization before GAS6 binding studies. • Kinase-dead rescue: K567R mutation in the ATP-binding lysine abolishes catalytic activity. • Bemcentinib-resistant rescue: gatekeeper mutations can confer bemcentinib resistance for on-target validation. • Functional readout: rescue should restore GAS6-induced phospho-AXL and downstream signaling. A-549 transduces efficiently with lentivirus and supports stable rescue line generation.