ADAM17 Knockout HEK293 Cell Line

The choice depends on whether you are studying ADAM17 (TACE, TNF-α converting enzyme)'s role as the principal sheddase for TNF-α and EGFR ligands or modeling its emerging cancer applications. The Knockout line is the standard tool for asking whether ADAM17 is required for these processes — ADAM17 is a metalloproteinase that cleaves and releases the extracellular domains of >80 substrates including: TNF-α (releasing soluble TNF-α from membrane-bound proTNF-α), EGFR ligands (TGF-α, amphiregulin, HB-EGF, epiregulin, epigen — driving autocrine/paracrine EGFR activation), IL-6R, L-selectin, Notch, CD16. ADAM17 activity is regulated by iRhoms (RHBDF1, RHBDF2) which control its maturation, trafficking, and substrate selectivity. Overexpression is useful for studying ADAM17 gain-of-function effects. For inflammation and cancer research, the EDITGENE ADAM17 Knockout in HEK293 is uniquely valuable — ADAM17 is one of the most clinically relevant metalloproteinases. This product complements the parallel iRhom (RHBDF1, RHBDF2, RHBDF1&2 double KO) products in EDITGENE for systematic ADAM17 regulation studies. Rescue with wild-type, catalytically-dead (E406A in metalloprotease active site), or substrate-binding-deficient ADAM17 enables structure-function studies. The knockout is a critical specificity tool for ⭐ TAPI-0/TAPI-1/TAPI-2 (classical ADAM17 inhibitors), ⭐ INCB7839 (aderbasib, dual ADAM10/17 inhibitor in clinical development for HER2+ breast cancer), MEDI3622 (anti-ADAM17 antibody), and emerging ADAM17-targeted inflammation and cancer therapeutics.

Primary applications: • TNF-α shedding: soluble TNF-α release analysis by ELISA from PMA-stimulated cells — abolished in ADAM17 KO. • EGFR ligand shedding: TGF-α, amphiregulin, HB-EGF, epiregulin, epigen shedding analysis given ADAM17's role in autocrine/paracrine EGFR activation. • iRhom regulation: parallel analysis with RHBDF1, RHBDF2, RHBDF1&2 double KO products in EDITGENE for systematic ADAM17 regulation studies. • ADAM17 inhibitor specificity: critical genetic control for ⭐ TAPI-0/1/2 (classical), ⭐ INCB7839/aderbasib (clinical dual ADAM10/17 inhibitor), MEDI3622 (anti-ADAM17 antibody). • TNF biology: in heterologous inflammation-relevant contexts, regulated TNF-α release studies. EDITGENE recommends this model as the gold-standard genetic specificity control for ADAM17 sheddase research and ADAM17-targeted inflammation/cancer drug development.

Yes. ADAM17 rescue experiments are well-established for sheddase research: • Construct design: use a codon-modified ADAM17 sequence with a small intracellular C-terminal tag (FLAG, HA). ADAM17 has prodomain (cleaved during maturation), metalloprotease catalytic domain (with active site zinc), disintegrin and cysteine-rich domain, transmembrane span, and intracellular tail — preserve membrane topology. • Surface localization validation: ADAM17 maturation requires iRhom (RHBDF1, RHBDF2) for ER exit — confirm plasma membrane ADAM17 by cell surface staining; rescue interpretation considers iRhom expression. • Catalytically-dead rescue: E406A in the metalloprotease catalytic glutamate abolishes proteolytic activity. • Prodomain-mutant rescue: prodomain processing site mutations affect maturation. • Functional readout: rescue should restore TNF-α and EGFR ligand shedding measured by ELISA. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.