Arachidonate 5-Lipoxygenase Proteins (ALOX5)

Human Arachidonate 5-Lipoxygenase (ALOX5) interaction partners

1. 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.

2. 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.

3. Indicate a potential protective role of ALOX5AP and 5-arachidonate lipoxygenase gene in diabetes type 2 pathogenesis.

4. 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.

5. the influence of TGFbeta/SMADs on MLL- and MLL-AF4-mediated 5-LO promoter activation

6. 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.

7. 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.

8. This study revealed that epistatic interaction among the ALOX5, ALOX5AP and MPO genes played a significant role in vulnerability to ischemic stroke.

9. 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

10. 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.

11. 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

12. 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.

13. Polymorphisms in the 5-Lipoxygenase is associated with Incident Myocardial Infarction.

14. our results define Alox5 as a key genetic effector of JAK2V617F in driving polycythemia vera

15. Adipose tissue eicosapentaenoic acid and arachidonic acid and the ALOX-5 tandem repeat polymorphism did not significantly interact to affect the risk of myocardial infarction.

16. coexpression of the isoforms inhibited or stimulated 5-LO-WT expression in transiently and stably transfected HEK293T cells suggesting that the isoforms have other functions than canonical leukotriene biosynthesis

17. a novel putative protein isoform of human 5-LO that lacks exon 4, termed 5-LODelta4, was identified.

18. Oxidative stress decreased the levels of PNPLA2 transcripts with no effect on ALOX5 expression. Exogenous additions of P1 peptide or overexpression of the PNPLA2 gene decreased both LTB4 levels and death of RPE cells undergoing oxidative stress.

19. Dimethyl ester of bilirubin exhibits anti-inflammatory activity through inhibition of secretory phospholipase A2, lipoxygenase and cyclooxygenase.

20. Copy number variation in ALOX5 is associated with NSAIDs-induced urticaria and/or angioedema.

Mouse (Murine) Arachidonate 5-Lipoxygenase (ALOX5) interaction partners

1. it was suggested that 5-LO in monocytes played a pivotal role in monocyte-macrophage differentiation and subsequent infiltration of macrophage in neointima, leading to vascular remodeling after vascular injury.

2. the up-regulation of the ALOX5 is responsible for the Homocysteine-dependent worsening of the Alzheimer's disease phenotype in a relevant mouse model of the disease.

3. Our data showed that besides the high parasite burden and lack of microbicidal molecules, an imbalance with high COX-2 and 5-LOX eicosanoid expression and a lack of regulatory PPAR-gamma cytoplasm-to-nucleus translocation in macrophages were observed in mice that develop cerebral malaria.

4. Data indicate that 5-lipoxygenase (5-LO)/leukotriene B4 (LTB4) axis orchestrates graft-versus-host disease (GVHD) development and suggest it could be a target for the development of therapeutic strategies for GVHD treatment.

5. Findings demonstrate that the up-regulation of the ALOX5 gene pathway is responsible for the development of the biochemical and behavioral sequelae of high Hcy brain levels in the context of a neurodegenerative phenotype.

6. This study demonstrates that LTB4 promotes macrophage phagocytosis of bacteria via BLT1, and that BLT2 can fulfill this role in the absence of BL

7. our results define Alox5 as a key genetic effector of JAK2V617F in driving polycythemia vera

8. Homocysteine directly influences 5LO expression levels and establish a previously unknown cross talk between these two pathways.

9. Dimethyl ester of bilirubin exhibits anti-inflammatory activity through inhibition of secretory phospholipase A2, lipoxygenase and cyclooxygenase.

10. Data suggest that miR-674-5p (microRNA-674-5p) serves as a negative regulator in 5-LO (arachidonate 5-lipoxygenase) mediated autoimmune liver injury; miR-674-5p represses expression of 5-LO in hepatocytes in the presence of IL-6 (interleukin-6) or TNFa (tumor necrosis factor-alpha).

11. Results establish a key role of 5-Lipoxygenase in the development of the tau pathology phenotype and demonstrate it to be a novel viable therapeutic target for the pharmacologic treatment of human tauopathy.

12. GSAP cleavage via caspase-3 is regulated and depend upon the availability of 5-Lipoxygenase in Alzheimer's disease.

13. SHH-responsive 5-lipoxygenase, 15-lipoxygenase and COX-2 modulate Dectin-1-induced inflammatory cytokines.

14. involvement of lipoxygenase pathways in TNF-alpha-induced production of cytokines and chemokines

15. explored the relationship between 5-LO and central and peripheral eosinophilia in an asthma model using PAS or BALB/c mice and 5-LO-deficient mutants

16. ALOX5 deficiency prevents stress-induced memory deficits, synaptic dysfunction and tauopathy in a mouse model of Alzheimer's disease.

17. 5-LO activation coordinates the inflammatory immune response involved in the control of visceral leishmaniasis.

18. 5-LO(-/-) mice subjected to kidney insult presented lower macrophage infiltration and higher levels of IL-10 than wild-type mice.

19. Alox5 affects the osteogenic and adipogenic abilities of iPSCs in vivo and the effect of Cox2 inhibition in this system.

20. Data show that resolvin D1 decrease nuclear 5-lipoxygenase (5-LOX) and the leukotrienes LTB4:LXA4 ratio by macrophages lacking calcium-sensitive kinase calcium-calmodulin-dependent protein kinase II (CaMKII).

Horse (Equine) Arachidonate 5-Lipoxygenase (ALOX5) interaction partners

1. [5-lipoxygenase; 5-lox] protein expression and enzyme activity of 5-LOX were significantly higher in horses harbouring encysted larvae in comparison with horses free of encysted larvae

2. Increased PGE2 production led to reduction in 5-LO products in LPS-treated equine whole blood via IL-1b.