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Data suggest that the KKK motif is a governor of 5-LOX enzyme activity and the helper protein FLAP is required to sufficiently relieve its auto-suppression for effective leukotrienes (LT) synthesis. Moreover, substrate sequestering and/or handoff by FLAP may limit the rate of LTA4 synthesis by the hyperactive triple K mutant.
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Human cytomegalovirus induced both COX-2 and 5-LO proteins but not transcripts in breast cancer.
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5-LOX does not react with 5,15-diHpETE, although it can produce lipoxin A4 when 15-HpETE is the substrate. In contrast, both 12-LOX and 15-LOX-1 react with 5,15-diHpETE, forming specifically lipoxin B4.
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High lox5 expression is associated with dysmenorrhea.
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Our study showed that ALOX5 rs12762303 was associated with fasting blood glucose (FBG) levels but not with myocardial infarction in Chinese population
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ALOX5 rs4987105 polymorphism is associated with type 2 diabetes.
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PFN1 down-regulated the expression of lipoxygenase arachidonate 5-lipoxygenase (ALOX5) in human endometrial stromal cells and THP-1 macrophages.
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our work shows that ALOX5 plays a moderate anti-tumor role and functions as a drug sensitizer, with a therapeutic potential, in MLL-rearranged AML.
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Study shows that higher COX-2 and ALOX5 expression in colorectal cancer (CRC) tissues was correlated with poorer prognosis in patients with CRC. Also, MiR-216a-3p was shown to directly bind to there 3'-UTR and inversely regulates their protein levels modulating CRC cell proliferation.
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Indicate a potential protective role of ALOX5AP and 5-arachidonate lipoxygenase gene in diabetes type 2 pathogenesis.
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Our data reveal that 5-LO, which is required for leukotriene production and subsequent T cell recruitment, is downregulated in TAMs through Mer tyrosine kinase-dependent recognition of apoptotic cancer cells.
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the influence of TGFbeta/SMADs on MLL- and MLL-AF4-mediated 5-LO promoter activation
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The knockdown of arachidonate 5-lipoxygenase (Alox5) gene can induce the decreased levels of bcl/abl mRNA and BCR/ABL fusion protein in the K562/ADM cells and increased apoptosis rate.
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Data suggest that the co-carcinogens benzidine and hydrogen peroxide induce expression of ALOX5 mRNA and protein in tracheobronchial epithelial cells; the co-carcinogens decrease cell proliferation but enhance apoptosis, actions inhibited by knockdown of ALOX5 by RNA interference. Benzidine appears to undergo metabolic activation to benzidine diimine by ALOX5.
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This study revealed that epistatic interaction among the ALOX5, ALOX5AP and MPO genes played a significant role in vulnerability to ischemic stroke.
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The anticancer effects by 13'-COOHs appeared to be partially independent of inhibition of COX-2/5-LOX. Using liquid chromatography tandem mass spectrometry, we found that 13'-COOHs increased intracellular dihydrosphingosine and dihydroceramides after short-time incubation in HCT-116 cells, and enhanced ceramides while decreased sphingomyelins during prolonged treatment
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ROS production induced by the 5-LO pathway mediates the anti-cancer effects of docosahexaenoyl ethanolamide and N-arachidonoyl-L-alanine on head and neck squamous cell carcinoma cells.
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Specific inhibitors of COX-2 and 5-LOX decreased formation of HKD2 and HKE2 Platelets did not form HKs from exogenous 5S-hydroxyeicosatetraenoic acid, implying that COX-1 is not involved
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The observation that the coexpression of FLAP with a subset of the 5-LOX mutants restores 5-LOX-wild-type (wt)-like levels of products formed in intact cells suggests a physical protein-protein interaction, beyond colocalization, of 5-LOX and FLAP.
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Polymorphisms in the 5-Lipoxygenase is associated with Incident Myocardial Infarction.