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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 Proteins (12) and many more products for this protein.
Showing 10 out of 67 products:
Human ALOX5 ELISA Kit for Sandwich ELISA - ABIN832344
van der Laan, Foroughi Asl, van den Borne, van Setten, van der Perk, van de Weg, Schoneveld, de Kleijn, Michoel, Björkegren, den Ruijter, Asselbergs, de Bakker, Pasterkamp: Variants in ALOX5, ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: the Athero-Express Genomics Study. in Atherosclerosis 2015
ROS (show ROS1 ELISA Kits) 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 (show COX2 ELISA Kits) and 5-LOX decreased formation of HKD2 and HKE2 (show PFDN6 ELISA Kits) Platelets did not form HKs from exogenous 5S-hydroxyeicosatetraenoic acid, implying that COX-1 (show COX1 ELISA Kits) is not involved
The observation that the coexpression of FLAP (show ALOX5AP ELISA Kits) 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 ELISA Kits).
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 ELISA Kits)
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.
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.
Dimethyl ester of bilirubin exhibits anti-inflammatory activity through inhibition of secretory phospholipase A2 (show YWHAZ ELISA Kits), lipoxygenase and cyclooxygenase.
Our data showed that besides the high parasite burden and lack of microbicidal molecules, an imbalance with high COX-2 (show COX2 ELISA Kits) and 5-LOX eicosanoid expression and a lack of regulatory PPAR-gamma (show PPARG ELISA Kits) 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 ELISA Kits)) 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 (show PTGR1 ELISA Kits) promotes macrophage phagocytosis of bacteria via BLT1, and that BLT2 (show LTB4R2 ELISA Kits) 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.
Data suggest that miR (show MLXIP ELISA Kits)-674-5p (microRNA-674-5p) serves as a negative regulator in 5-LO (arachidonate 5-lipoxygenase) mediated autoimmune liver injury; miR (show MLXIP ELISA Kits)-674-5p represses expression of 5-LO in hepatocytes in the presence of IL-6 (interleukin-6 (show IL6 ELISA Kits)) or TNFa (tumor necrosis factor-alpha (show TNF ELISA Kits)).
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 ELISA Kits) cleavage via caspase-3 (show CASP3 ELISA Kits) 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