ERBB2 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying ERBB2 (HER2, Neu)'s role as the principal heterodimerization partner of the EGFR/ERBB family or modeling HER2-amplified breast cancer and HER2-targeted therapy. The Knockout line is the standard tool for asking whether HER2 is required for these processes — ERBB2 is the orphan receptor of the EGFR family (no high-affinity ligand identified) that preferentially heterodimerizes with EGFR (ERBB1), ERBB3, and ERBB4 to amplify ligand-induced signaling; HER2 amplification (~20% of breast cancers, also gastric cancer, esophageal adenocarcinoma, NSCLC) is one of the most clinically actionable oncogenic events. Overexpression is useful for studying HER2 amplification effects. For HER2-targeted therapy research, the EDITGENE ERBB2 Knockout in HEK293 is uniquely valuable — HEK293 supports systematic structure-function studies of HER2 and serves as a critical specificity control for HER2-targeted compound development. Rescue with wild-type, kinase-dead, or specific HER2 variants enables structure-function studies. The knockout is a critical specificity tool for ⭐⭐⭐ trastuzumab (Herceptin), pertuzumab (Perjeta), trastuzumab emtansine (T-DM1, Kadcyla), trastuzumab deruxtecan (T-DXd, Enhertu — also active in HER2-low breast cancer), tucatinib (Tukysa), neratinib, lapatinib, and emerging HER2-targeted ADC/bispecific antibody/CAR-T strategies — HER2 is one of the most validated cancer drug targets.

Primary applications: • HER2-targeted therapy specificity: critical genetic control for trastuzumab (Herceptin), pertuzumab (Perjeta), trastuzumab emtansine (T-DM1, Kadcyla), trastuzumab deruxtecan (T-DXd, Enhertu). • HER2 kinase inhibitor specificity: tucatinib (Tukysa), neratinib (Nerlynx), lapatinib (Tykerb) specificity testing. • ERBB heterodimerization: ERBB1/EGFR, ERBB3, ERBB4 heterodimer formation analysis given HER2's preferred heterodimerization partner role. • HER2-low cancer biology: in heterologous breast cancer-relevant contexts, T-DXd (Enhertu, which works in HER2-low cancer) mechanism studies. EDITGENE recommends this model as the gold-standard genetic specificity control for HER2-targeted breast cancer, gastric cancer, and emerging HER2-low/HER2-overexpressing cancer drug development.

Yes. HER2 rescue experiments are well-established for cancer drug development: • Construct design: use a codon-modified ERBB2 sequence with a small intracellular C-terminal tag (FLAG, HA). HER2 has extracellular four-domain region (subdomains I-IV, with pertuzumab binding subdomain II and trastuzumab binding subdomain IV), single transmembrane span, juxtamembrane region, and intracellular kinase domain — preserve all elements. • Surface localization validation: confirm plasma membrane HER2 expression before therapy specificity testing. • Kinase-dead rescue: K753A in the ATP-binding lysine abolishes catalytic activity. • Trastuzumab-resistant rescue: subdomain IV epitope mutations confer trastuzumab resistance for on-target Herceptin validation. • Functional readout: rescue should restore HER2 heterodimerization with EGFR/ERBB3/ERBB4, downstream PI3K-AKT/MAPK signaling, and HER2-targeted therapy sensitivity. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.