ALOX12

(redirected from 12-LOX)

ALOX12

A gene on chromosome 17p13.1 that encodes a member of the lipoxygenase (LOX) family of non-heme iron dioxygenases, which are involved in the production and metabolism of fatty acid hydroperoxidases.
References in periodicals archive ?
This study also shows that maresin 1 exhibits novel mechanisms in the resolution of inflammation in that it can inhibit proinflammatory mediator production by LTA4 hydrolase and can block arachidonate conversion by human 12-LOX, rather than merely terminating phagocyte involvement [20].
COX pathways consist of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), while 5-lipoxygenase (5-LOX), 12-lipoxygenase (12-LOX), and 15-lipoxygenase (15-LOX) are the examples of the LOX pathway.
Like 5-LOX, inhibition of 12-LOX also reduced the numbers of living HCC cells by increasing apoptosis and reducing proliferation (Xu et al., 2012).
Apart from the absolute belief of 15-RHETE being a sole product, as derived by the acetylation of COX-2, the presence of the double dioxygenated product, 5S12S-DiHETE isolated in vivo, suggests further transcellular metabolic events that show further eicosanoid synthesis by 5- and 12-LOX interactions [31].
The team found that dietary fructose and sucrose increased 12-lipoxygenase (12-LOX) signaling, which increased production of 12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE) to raise the risk of breast cancer development and metastasis.
"This was due, in part, to increased expression of 12-LOX and a related fatty acid called 12-HETE."
"This was due, in part, to increased expression of 12-LOX [which plays a role in cell death] and a related fatty acid called 12-HETE."
A study funded by the National Institutes of Health was published recently in the Journal of Cerebral Blood Flow and Metabolism, shedding light on how tocotrienol, a 12-Lox inhibitor, acts to confer neuroprotection post-stroke.
In humans, the term 12/15-LOX refers to leukocyte-type 12-LOX and-reticulocyte-type 15-LOX-1 since they produce the similar lipid mediators such as 12-and 15-hydroperoxyeicosatetraenoic acids (HPETEs) and hydroxyeicosatetraenoic acids (HETEs).
Therefore, knipholone showed higher affinity for the 5-LOX pathway than for cycloxygenases and 12-LOX.
These effects were diminished by PLA2 inhibitor (quinacrine), general LOX inhibitors (NDGA, ETYA), 5-LOX inhibitors (Rev 5901, AA861), 12-LOX inhibitor (baicalein) and FLAP inhibitor (MK886), while COX inhibitor (indomethacin) was without effect.
To the best of our knowledge, this is the first report of lichen compounds being investigated for 12-LOX inhibitory properties.