EGF Knockout Cell Line (HEK 293)

The choice depends on whether you are studying EGF (epidermal growth factor)'s role as the prototypical EGFR ligand or its functions in autocrine/paracrine signaling. The Knockout line is the standard tool for asking whether EGF is required for autocrine EGFR signaling — EGF is a 53-amino-acid secreted growth factor (processed from the larger pre-pro-EGF precursor) that binds EGFR (ERBB1) with high affinity, triggering receptor dimerization, autophosphorylation, and downstream PI3K-AKT and RAS-MAPK signaling. Overexpression is useful for studying EGF gain-of-function effects. For EGF-EGFR pathway research, the EDITGENE EGF Knockout in HEK293 enables study of autocrine EGF production. Rescue with wild-type or receptor-binding-deficient EGF enables structure-function studies. The knockout is valuable for studying autocrine EGF signaling, EGFR-targeted cancer therapeutic specificity (cetuximab, panitumumab anti-EGFR antibodies; gefitinib, erlotinib, osimertinib EGFR-TKIs), and emerging EGF-modulating therapeutic strategies.

Primary applications: • EGF secretion: secreted EGF quantification by ELISA in conditioned media to characterize autocrine EGF production. • Autocrine EGFR signaling: phospho-EGFR (Y1068, Y1173), phospho-ERK analysis in EGF-null cells. • Anti-EGFR therapy specificity: complementary specificity control for cetuximab (Erbitux), panitumumab (Vectibix) anti-EGFR antibody specificity testing. • EGFR-TKI mechanism: gefitinib, erlotinib, osimertinib mechanism studies with reduced autocrine EGF. EDITGENE recommends this model for researchers investigating EGF biology, autocrine EGFR signaling, and EGF-EGFR pathway therapeutic development.

Yes. EGF rescue experiments require attention to secreted growth factor processing: • Construct design: EGF is processed from a large pre-pro-EGF precursor (1207 aa) into the mature 53-aa secreted polypeptide — use untagged EGF and quantify secreted form by ELISA, or use precursor with internal tag carefully placed away from the EGF domain. • Secretion validation: confirm conditioned media EGF levels by ELISA before functional assays. • Receptor-binding-deficient rescue: EGFR-binding residue mutations in the mature EGF abolish EGFR activation. • Functional readout: rescue should restore conditioned-media EGF levels and autocrine EGFR activation. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.