EC Number   |
General Information |
Reference |
|---|
    1.13.11.33 | evolution |
gene ALOX15 encodes for human 15-LOX type 1 and murine 12/15-LOX. Although the encoded enzymes display slightly different specificities (15- versus 12-lipoxygenating activity), these proteins represent evolutionary and functionally closely-related enzymes that share a high degree of sequence similarity. Of note, these 12/15LOXs that are encoded by the ALOX15 genes have separated from other LOXs early during evolution, although they share close biochemical properties with other LOXs such as ALOX12 or ALOX15B |
742000 |
| 1.13.11.33 | evolution |
LOX isozymes and classification systems, overview |
742613 |
| 1.13.11.33 | evolution |
mammals (mice, rats, pigs) express 12-lipoxygenating ALOX15 orthologues. 15-lipoxygenating isoforms are found in primates (orangutans, humans), suggesting an evolution of ALOX15 specificity. Other primates (baboons, rhesus monkeys) express 12-lipoxygenating enzymes. Gibbons, which are flanked in evolution by rhesus monkeys (12-lipoxygenating ALOX15) and orangutans (15-lipoxygenating ALOX15), express an ALOX15 ortholog with pronounced dual specificity, an evolution of ALOX15 specificity, which is aimed at optimizing the biosynthetic capacity for antiinflammatory and proresolving lipoxins. Phylogenetic analysis |
743691 |
| 1.13.11.33 | malfunction |
Alox15 deletion impaired LSC function by affecting cell division and apoptosis, leading to an eventual depletion of leukemia stem cells. Chemical inhibition of enzyme 15-LO function impairs leukemia stem cell function and attenuates chronic myeloid leukemia in mice. The defective chronic myeloid leukemia phenotype in Alox15-deficient animals is rescued by depleting the gene encoding P-selectin, which is upregulated in Alox15-deficient animals. Both deletion and overexpression of P-selectin affects the survival of leukemia stem cells. Loss of Alox15 causes a functional defect in leukemia stem cells |
742977 |
| 1.13.11.33 | malfunction |
deletion of 12/15-LO negates endothelial tight junctions disruption and monocyte adhesion caused by the high-fat diet |
-, 742845 |
| 1.13.11.33 | malfunction |
disruption of normal 12- and 15-LO function by the inflammatory obese condition promotes adipocyte dysfunction and overall metabolic disease including insulin resistance and diabetes |
743718 |
| 1.13.11.33 | malfunction |
streptozotocin (STZ)-induced diabetic mice show upregulated expression of 12/15-LOX and inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and nuclear factor (NF)-kappaB in diabetic hearts. Disruption of 12/15-LOX significantly improves STZ-induced cardiac dysfunction and fibrosis. Deletion of 12/15-LOX inhibits the increases of TNF-alpha and NF-kappaB as well as the production of STZ-induced reactive oxygen species in the heart. Administration of N-acetylcysteine in diabetic mice prevents STZ-induced cardiac fibrosis. Neonatal cultured cardiomyocytes exposed to high glucose conditions induce the expression of 12/15-LOX as well as TNF-alpha, NF-kappaB, and collagen markers. These increases are inhibited by treatment of the 12/15-LOX inhibitor. Disruption of 12/15-LOX reduces inflammation, oxidative stress, and fibrosis in the diabetic heart, thereby improving systolic dysfunction. Disruption of 12/15-LOX decreases cardiac inflammation induced by hyperglycemia |
-, 742346 |
| 1.13.11.33 | malfunction |
when 15-LOX-1 activity is knocked down by siRNA, the induction of MIP-1alpha, RANTES, and IP-10 is significantly attenuated |
701633 |
| 1.13.11.33 | metabolism |
cardiac 12/15-LOX pathway induced by high glucose condition increases the expression of cardiac inflammation in vitro |
742346 |
| 1.13.11.33 | metabolism |
shifting linoleic acid metabolism from 15-LOX-1 to COX-2 is procarcinogenic |
706877 |
