ALOX5 Knockout Cell Line (HEK293)

The choice depends on whether you are studying ALOX5 (5-lipoxygenase, 5-LOX)'s role as the principal leukotriene-synthesizing enzyme or modeling asthma and emerging cancer applications. The Knockout line is the standard tool for asking whether 5-LOX is required for these processes — ALOX5 catalyzes the conversion of arachidonic acid to 5-HPETE and subsequently to LTA4 (in concert with FLAP/ALOX5AP), the precursor of all leukotrienes; 5-LOX is critical for neutrophil/eosinophil activation, bronchoconstriction in asthma, and atherosclerosis. Overexpression is useful for studying 5-LOX gain-of-function effects. For leukotriene biology research, the EDITGENE ALOX5 Knockout in HEK293 is uniquely valuable for studying the principal leukotriene-synthesizing enzyme. This product complements the parallel ALOX5AP/FLAP Knockout in HEK293 (also available) for systematic 5-LOX pathway dissection. Rescue with wild-type or catalytically-dead ALOX5 enables structure-function studies. The knockout is a critical specificity tool for ⭐ zileuton (Zyflo, FDA-approved 5-LOX inhibitor for asthma), MK-0633, and emerging 5-LOX-targeted approaches; CysLT1 receptor antagonists (montelukast/Singulair, zafirlukast) target the downstream cysteinyl leukotriene pathway.

Primary applications: • Leukotriene synthesis: 5-HPETE and downstream leukotriene quantification — completely abolished in ALOX5 KO. • Zileuton specificity: critical genetic control for zileuton (FDA-approved asthma 5-LOX inhibitor) — should have no inhibitory effect in ALOX5-null cells. • 5-LOX/FLAP pathway dissection: paired analysis with ALOX5AP/FLAP KO in HEK293 (also available). • Atherosclerosis biology: in heterologous macrophage-relevant contexts, 5-LOX's role in atherosclerosis. EDITGENE recommends this ALOX5 KO paired with FLAP KO for systematic 5-LOX leukotriene research.

Yes. ALOX5 rescue experiments are well-established for leukotriene biology: • Construct design: use a codon-modified ALOX5 sequence with a small C-terminal tag (FLAG, HA). ALOX5 has N-terminal C2-like (calcium/membrane binding) and C-terminal catalytic domain with active site iron — preserve all elements. • Catalytically-dead rescue: H367A/H372A/H550A iron-binding histidine mutations abolish lipoxygenase activity. • Zileuton-resistant rescue: gatekeeper or specific active site mutations can confer zileuton resistance for on-target validation. • Functional readout: rescue should restore 5-HPETE and leukotriene synthesis in arachidonic acid-stimulated cells. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.