HGF Knockout Cell Line (HEK 293)

The choice depends on whether you are studying HGF (hepatocyte growth factor)'s role as the c-MET (HGFR) ligand or modeling its autocrine/paracrine functions in cancer and tissue regeneration. The Knockout line is the standard tool for asking whether HGF is required for autocrine c-MET signaling — HGF is a 90 kDa secreted heterodimeric growth factor (α and β chains processed from a single precursor) that binds c-MET receptor tyrosine kinase with high affinity, driving PI3K-AKT, MAPK, and other downstream signaling for cell proliferation, motility (scattering), and survival. Overexpression is useful for studying HGF gain-of-function effects. For HGF-MET pathway research, the EDITGENE HGF Knockout in HEK293 enables study of autocrine HGF production. Rescue with wild-type or proteolytic-cleavage-deficient HGF (HGF requires HGF activator/HGFA cleavage between the α and β chains for biological activity) enables structure-function studies. The knockout is valuable for studying HGF-MET autocrine signaling, MET-targeted cancer therapeutics (capmatinib, tepotinib, savolitinib FDA-approved for METex14 NSCLC; anti-HGF antibody rilotumumab in development), and HGF's role in liver regeneration and fibrosis.

Primary applications: • HGF secretion: secreted HGF quantification by ELISA in conditioned media to characterize autocrine HGF production. • Autocrine c-MET activation: phospho-c-MET (Y1234/Y1235) and downstream PI3K-AKT/MAPK analysis in HGF-null cells with c-MET-expressing background. • HGF-MET cancer therapy: capmatinib (FDA-approved for METex14 NSCLC), tepotinib, savolitinib mechanism studies given the HGF-MET axis in cancer. • Anti-HGF antibody specificity: rilotumumab and other anti-HGF therapeutic antibody specificity control. EDITGENE recommends this model for researchers investigating HGF-MET signaling, autocrine HGF production, and HGF-MET-targeted cancer therapeutic development.

Yes. HGF rescue experiments require attention to secreted heterodimeric growth factor processing: • Construct design: HGF is a secreted protein processed from a single precursor into α and β chains held by disulfide bonds — N-terminal tag (after signal peptide) is preferred over C-terminal which can disrupt processing. • Secretion validation: confirm conditioned media HGF levels by ELISA before functional assays. • Activation-deficient rescue: HGF requires HGFA (HGF activator) protease cleavage between α and β chains for biological activity — uncleavable HGF mutants generate latent/inactive HGF. • Functional readout: rescue should restore conditioned-media HGF levels and autocrine c-MET activation. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.