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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 (212) and ALOX5 Proteins (13) and many more products for this protein.
Showing 10 out of 73 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
Human ALOX5 ELISA Kit for Sandwich ELISA - ABIN414629
Kapral, Wawszczyk, Sośnicki, Jesse, Węglarz: Modulating effect of inositol hexaphosphate on arachidonic acid-dependent pathways in colon cancer cells. in Prostaglandins & other lipid mediators 2017
Our data reveal that 5-LO, which is required for leukotriene production and subsequent T cell recruitment, is downregulated in TAMs through Mer (show MERTK ELISA Kits) tyrosine kinase (show TXK ELISA Kits)-dependent recognition of apoptotic cancer cells.
the influence of TGFbeta (show TGFB1 ELISA Kits)/SMADs on MLL- and MLL-AF4-mediated 5-LO promoter activation
The knockdown of arachidonate 5-lipoxygenase (Alox5) gene can induce the decreased levels of bcl/abl (show ABL1 ELISA Kits) mRNA and BCR/ABL (show ABL1 ELISA Kits) fusion protein in the K562/ADM (show ADM ELISA Kits) cells and increased apoptosis rate.
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.
This study revealed that epistatic interaction among the ALOX5, ALOX5AP (show ALOX5AP ELISA Kits) and MPO (show MPO ELISA Kits) 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 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.
Results indicate 15-lipoxygenase modified LDL as a new inducer for LOX-1 (show OLR1 ELISA Kits) expression and as a new ligand for LOX-1 (show OLR1 ELISA Kits).
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 promotes macrophage phagocytosis of bacteria via BLT1, and that BLT2 can fulfill this role in the absence of BL
our results define Alox5 as a key genetic effector of JAK2V617F in driving polycythemia vera (show IGF2BP3 ELISA Kits)
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 ELISA Kits), lipoxygenase and cyclooxygenase.
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.
[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
Increased PGE2 production led to reduction in 5-LO products in LPS-treated equine whole blood via IL-1b (show IL1B ELISA Kits).
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.
, 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
, erythroid cell-specific 15-lipoxygenase
, omega-6 lipoxygenase
, 5 - Lipoxygenase
, arachidonate 5-lipoxygenase
, Arachidonate 5-lipoxygenase