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ALOX5 encodes a member of the lipoxygenase gene family and plays a dual role in the synthesis of leukotrienes from arachidonic acid. Additionally we are shipping ALOX5 Antibodies (201) and ALOX5 Kits (67) and many more products for this protein.
Showing 10 out of 12 products:
This study revealed that epistatic interaction among the ALOX5, ALOX5AP (show ALOX5AP Proteins) and MPO (show MPO Proteins) genes played a significant role in vulnerability to ischemic stroke.
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
ROS (show ROS1 Proteins) 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.
Specific inhibitors of COX-2 and 5-LOX decreased formation of HKD2 and HKE2 (show PFDN6 Proteins) Platelets did not form HKs from exogenous 5S-hydroxyeicosatetraenoic acid, implying that COX-1 is not involved
The observation that the coexpression of FLAP (show ALOX5AP Proteins) 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 (show ALOX5AP Proteins).
Polymorphisms in the 5-Lipoxygenase is associated with Incident Myocardial Infarction.
our results define Alox5 as a key genetic effector of JAK2V617F in driving polycythemia vera (show IGF2BP3 Proteins)
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.
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
a novel putative protein isoform of human 5-LO that lacks exon 4, termed 5-LODelta4, was identified.
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 (show PPARG Proteins) cytoplasm-to-nucleus translocation in macrophages were observed in mice that develop cerebral malaria.
Data indicate that 5-lipoxygenase (5-LO)/leukotriene B4 (LTB4 (show PTGR1 Proteins)) axis orchestrates graft-versus-host disease (GVHD) development and suggest it could be a target for the development of therapeutic strategies for GVHD treatment.
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.
This study demonstrates that LTB4 promotes macrophage phagocytosis of bacteria via BLT1, and that BLT2 can fulfill this role in the absence of BL
Homocysteine directly influences 5LO expression levels and establish a previously unknown cross talk between these two pathways.
Dimethyl ester of bilirubin exhibits anti-inflammatory activity through inhibition of secretory phospholipase A2 (show YWHAZ Proteins), lipoxygenase and cyclooxygenase.
Data suggest that miR (show MLXIP Proteins)-674-5p (microRNA-674-5p) serves as a negative regulator in 5-LO (arachidonate 5-lipoxygenase) mediated autoimmune liver injury; miR (show MLXIP Proteins)-674-5p represses expression of 5-LO in hepatocytes in the presence of IL-6 (interleukin-6 (show IL6 Proteins)) or TNFa (tumor necrosis factor-alpha (show TNF Proteins)).
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.
GSAP (show PION Proteins) cleavage via caspase-3 (show CASP3 Proteins) is regulated and depend upon the availability of 5-Lipoxygenase in Alzheimer's disease.
This gene encodes a member of the lipoxygenase gene family and plays a dual role in the synthesis of leukotrienes from arachidonic acid. The encoded protein, which is expressed specifically in bone marrow-derived cells, catalyzes the conversion of arachidonic acid to 5(S)-hydroperoxy-6-trans-8,11,14-cis-eicosatetraenoic acid, and further to the allylic epoxide 5(S)-trans-7,9-trans-11,14-cis-eicosatetrenoic acid (leukotriene A4). Leukotrienes are important mediators of a number of inflammatory and allergic conditions. Mutations in the promoter region of this gene lead to a diminished response to antileukotriene drugs used in the treatment of asthma and may also be associated with atherosclerosis and several cancers. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, arachidonate 5-lipoxygenase
, Arachidonate 5-lipoxygenase
, arachidonic 5-lipoxygenase alpha-10 isoform
, arachidonic 5-lipoxygenase delta-10-13 isoform
, arachidonic 5-lipoxygenase delta-13 isoform
, arachidonic 5-lipoxygenase delta-p10 isoform
, arachidonic acid 5-lipoxygenase
, leukotriene A4 synthase
, 5 - Lipoxygenase