Arachidonate 5-Lipoxygenase Proteins (ALOX5)

Human Arachidonate 5-Lipoxygenase (ALOX5) interaction partners

1. Human cytomegalovirus induced both COX-2 and 5-LO proteins but not transcripts in breast cancer.

2. 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.

3. High lox5 expression is associated with dysmenorrhea.

4. Our study showed that ALOX5 rs12762303 was associated with fasting blood glucose (FBG) levels but not with myocardial infarction in Chinese population

5. ALOX5 rs4987105 polymorphism is associated with type 2 diabetes.

6. PFN1 down-regulated the expression of lipoxygenase arachidonate 5-lipoxygenase (ALOX5) in human endometrial stromal cells and THP-1 macrophages.

7. 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.

8. 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.

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

10. 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.

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

12. 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.

13. 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.

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

15. 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

16. 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.

17. 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

18. 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.

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

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

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

1. that 5-lipoxygenase directly modulates tau phosphorylation at the same epitopes via the cdk5 kinase pathway

2. Data show that the 5-Lipoxygenase knockout mice (5-LO(-/-) wounds had diminished mRNA expression in the skin lesions.

3. Within the endothelial population, cells that transition from haemogenic endothelial to erythro-myeloid progenitors specifically express Alox5 and its co-factor Alox5ap, which control leukotriene production. Functional assays using mouse embryonic stem cells demonstrate that leukotrienes promote haematopoietic progenitor cell generation.

4. neuronal 5LO is directly involved in tau phosphorylation and tau neuropathology.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

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

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

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

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

14. 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).

15. 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.

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

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

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

19. 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

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

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.