RHBDF2 Knockout Cell Line (A549)

The choice depends on whether you are studying RHBDF2 (iRhom2)'s role in lung cancer biology and EGFR ligand shedding or its functions in respiratory epithelial TACE regulation. The Knockout line is appropriate for asking whether iRhom2 is required for ADAM17-mediated EGFR ligand shedding (TGF-α, amphiregulin, heparin-binding EGF) in lung cancer contexts — particularly relevant in A-549, an NSCLC model. Overexpression is useful for studying iRhom2 in lung cancer progression. For lung cancer and EGFR signaling research, the EDITGENE RHBDF2 Knockout in A-549 is highly relevant — A-549 expresses EGFR pathway components and iRhom2-mediated shedding regulates autocrine/paracrine EGFR ligand availability. This product complements the parallel RHBDF2 Knockout in HEK293 and the RHBDF1 & RHBDF2 Double Knockout in A-549; the lung cancer context is preferred for disease-relevant studies. Rescue with wild-type or disease-associated (tylosis with esophageal cancer) iRhom2 enables genotype-function studies in a cancer-relevant background.

Primary applications: • EGFR ligand shedding: TGF-α, amphiregulin, heparin-binding EGF release in conditioned media to assess iRhom2-dependent shedding in lung cancer context. • Autocrine EGFR signaling: phospho-EGFR and downstream pathway activation analysis given iRhom2's role in regulating EGFR ligand availability. • Lung cancer proliferation: assessment of iRhom2-dependent EGFR autocrine loops on NSCLC proliferation and migration. • EGFR-targeted therapy interaction: cetuximab, erlotinib sensitivity studies in iRhom2-null versus rescued lung cancer cells. EDITGENE recommends this A-549-based model for lung cancer EGFR signaling research; the parallel knockout in HEK293 and double knockouts complement this for biochemistry and paralog studies.

Yes. iRhom2 rescue experiments in A-549 are well-suited for lung cancer ADAM17 research: • Construct design: use a codon-modified RHBDF2 sequence with a small C-terminal tag (FLAG, HA). Preserve the 7-transmembrane rhomboid family architecture. • Lung cancer-relevant rescue: TOC-associated and other RHBDF2 disease variants in lung cancer context for genotype-function studies relevant to esophageal cancer biology overlap. • ADAM17 substrate-specific rescue: rescue should restore EGFR ligand shedding (TGF-α, amphiregulin) measured in conditioned media by ELISA. • Functional readout: rescue should restore lung cancer-relevant ADAM17 substrate ectodomain shedding and downstream EGFR autocrine signaling. A-549 transduces efficiently with lentivirus and supports stable rescue line generation.