ALOX12B Knockout Cell Line (HEK293)

The choice depends on whether you are studying ALOX12B (12R-lipoxygenase, 12R-LOX)'s role in epidermal lipid biology or modeling autosomal recessive congenital ichthyosis (ARCI). The Knockout line is the standard tool for asking whether ALOX12B is required for these processes — ALOX12B catalyzes the conversion of arachidonic acid (or its ester forms in the ω-3 hydroxyceramide pathway) to 12R-HPETE; in epidermal lipid metabolism, ALOX12B works sequentially with ALOXE3 to generate hepoxilin A3 and other epidermal lipid mediators essential for skin barrier formation. Overexpression is useful for studying ALOX12B gain-of-function effects. For skin biology research, the EDITGENE ALOX12B Knockout in HEK293 is highly informative — ALOX12B biallelic loss-of-function mutations cause ⭐ autosomal recessive congenital ichthyosis (ARCI, particularly non-bullous congenital ichthyosiform erythroderma form). This product complements the parallel ALOXE3 Knockout in HEK293 (also available) for studying the ALOX12B-ALOXE3 epidermal lipoxygenase pathway. Rescue with wild-type or catalytically-dead ALOX12B enables structure-function studies. The knockout is valuable for studying epidermal lipid biology, skin barrier formation, and ichthyosis disease mechanisms.

Primary applications: • 12R-HPETE synthesis: 12R-HPETE and related epidermal lipid analysis by LC-MS. • ARCI modeling: rescue with patient-derived ALOX12B mutations for autosomal recessive congenital ichthyosis disease modeling. • ALOX12B-ALOXE3 sequential biology: paired analysis with ALOXE3 KO in HEK293 (also available) for complete epidermal lipoxygenase pathway dissection. • Skin barrier formation: epidermal lipid biology in heterologous keratinocyte-relevant contexts. EDITGENE recommends this ALOX12B KO paired with ALOXE3 KO for systematic epidermal lipoxygenase pathway research.

Yes. ALOX12B rescue experiments are well-established for epidermal lipid research: • Construct design: use a codon-modified ALOX12B sequence with a small C-terminal tag (FLAG, HA). ALOX12B has the canonical lipoxygenase architecture with active site iron — preserve all elements. • Catalytically-dead rescue: iron-binding histidine mutations abolish 12R-lipoxygenase activity. • ARCI patient mutation rescue: patient-derived ALOX12B mutations enable disease modeling. • Functional readout: rescue should restore 12R-HPETE synthesis from arachidonic acid substrate. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.