The Arachidonate 5-lipoxygenase (ALOX5) gene encodes 5-Lipoxygenase (5-LO), a key member of the fatty acid oxidase gene family. 5-LO is one of the crucial enzymes in the metabolic pathway of arachidonic acid (AA), an essential fatty acid in humans. It catalyzes the conversion of AA into leukotrienes (LTs), which are important mediators of various inflammatory and allergic diseases. ALOX5 is specifically expressed in bone marrow-derived cells and is significantly upregulated in myeloid leukemia stem cells, playing a pivotal role in the development of myeloid leukemia. Mutations in the promoter region of this gene weaken the response to leukotriene antagonists used for asthma treatment and are also associated with atherosclerosis and some cancers. Multiple splice variants encoding different isoforms have been identified for this gene.

This strain is a mouse Alox5 gene deletion model, achieved by using gene editing technology to knock out the homologous gene of human ALOX5 in mice. According to literature reports, these mice exhibit increased total adipose tissue weight, plasma VLDL/LDL cholesterol, and bone mineral density. Their spleens are typically smaller than those of wild-type mice, and they exhibit reduced inflammatory responses and abnormalities in immunophysiology^[1-3]. These homozygous Alox5 KO mice are viable and fertile.