EC Number   |
General Information |
Reference |
|---|
    1.13.11.31 | 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 |
| 1.13.11.31 | 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 |
| 1.13.11.31 | malfunction |
12-LOX inhibition attenuates platelet aggregation |
728826 |
| 1.13.11.31 | malfunction |
12-LOX-overexpressing PC-3 cells show an enhanced invasive ability which results from an increase in MMP9 expression and secretion |
727634 |
| 1.13.11.31 | malfunction |
ALOX12 expression and its metabolite 12(S)-hydroxyeicosatetraenoic acid are significantly increased in the visceral adipose tissue of type 2 diabetes subjects with body mass index of 21 |
742976 |
| 1.13.11.31 | malfunction |
cells with RNAi silenced 12/15-LO and stimulated with PDGF show an impaired STAT3 phosphorylation compared to cells transfected with the scrambled control |
727969 |
| 1.13.11.31 | malfunction |
deletion of 12/15-LOX in mice leads to increased cytochrome P450-derived bioactive lipid mediator epoxyeicosatrienoic acids, i.e. 11,12-EpETrE and 14,15-EpETrE, which are further enhanced by acute PUFA intake post-MI. Macrophage density is decreased in wild-type + PUFA and 12/15-LOX-/- mice compared with their respective standard diet-fed wild-type controls at day 5 post-MI. 12/15-LOX-/- + PUFA mice display an increased expression of chemokine (C-C motif) ligand 2 and reparative macrophages markers (Ym-1, Mrc-1, and Arg-1) in the infarcted area. Furthermore, 12/15-LOX-/- mice, with or without PUFA, show reduced collagen deposition at day 5 post-MI compared with wild-type mice. In conclusion, deletion of 12/15-LOX and short-term exposure of PUFA promote leukocyte clearance, thereby limiting cardiac remodeling and promoting an effective resolution of inflammation |
-, 741573 |
| 1.13.11.31 | 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 |
| 1.13.11.31 | malfunction |
macrophages that lack 12/15LO have enhanced transporter expression, reduced ATP-binding cassette G1 phosphorylation, and increased cholesterol efflux |
704567 |
| 1.13.11.31 | malfunction |
pharmacologic inhibition of 12-LOX in human platelets results in significant attenuation of FcgammaRIIa-mediated aggregation. Activation of the FcgammaRIIa receptor leads to immune-mediated thrombosis, which is often life threatening in patients undergoing heparin-induced thrombocytopenia or sepsis. Inhibiting FcgammaRIIa-mediated activation, e.g. by inhibiting the enzyme 12-LOX, in platelets limits thrombosis and is the principal target for prevention of immune-mediated platelet activation |
742190 |
