Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
The crystal structure of a mammalian 12-lipoxygenase reveals a plausible substrate access channel for oxygen.
12/15-Lipoxygenase activity increases the degradation of macrophage ATP-binding cassette transporter G1.
EPR (show EREG Proteins) spectroscopy and electrospray mass spectroscopy reveal distinctive features of the iron site in leukocyte arachidonate 12-lipoxygenase (show ALOX12 Proteins).
Results suggest an evolution of ALOX15 (12/15-lipoxygenase)specificity.
Compound heterozygous mutations in DYNC2H1 and ALOX15 were identified in miscarriages from two families with RPL. DYNC2H1 is involved in cilia biogenesis and has been associated with fetal lethality in humans. ALOX15 is expressed in placenta and its dysregulation has been associated with inflammation, placental, dysfunction, abnormal oxidative stress response and angiogenesis.
Immunofluorescence analyses revealed that the ALOX15 protein consistently localizes to cell membrane during the course of ferroptosis. Importantly, treatments of cells with ALOX15-activating compounds accelerated cell death at low, but not high doses of erastin and RSL3
present in late-stage germ cells of the testis
Studied human umbilical cord mesenchymal stem cell (hucMSCs) transplantation in DSS (show NR0B1 Proteins)-induced inflammatory bowel disease (IBD); hucMSC transplantation significantly relieved IBD symptoms thru the regulation of 15-LOX-1 expression and modulation of inflammatory responses in macrophages.
These results indicated that 15-LOX-1 is a potential target for inhibiting the trafficking of DCs to lymphoid organs and inflamed tissues and decreasing the inflammatory response attenuating symptoms of certain immunologic and inflammatory disorders such as dermatitis.
Kelavkar and Badr (1999) stated that the ALOX15 gene maps to 17p13.3 in close proximity to the tumor-suppressor gene TP53 (show TP53 Proteins) and stated that the ALOX15 gene product is implicated in antiinflammation, membrane remodeling, and cancer development/metastasis.
we propose that increased ALOX15 expression in heart tissue under ischemic conditions may lead to increased production of 15-HETE, potentially contributing to thrombosis.
the results of the present study indicated that the natural products, CA, quercetin and morin hydrate, offer potential as adjuvant therapeutic agents for SMinduced toxicity, not only by reducing inflammation mediated by the p38 (show CRK Proteins) and LOX (show LOX Proteins) signaling pathways, but also by decreasing the generation of ROS (show ROS1 Proteins) and nitrate/nitrite.
15-LOX-1 re-expression downregulates the expression of MTA1 (show MTA1 Proteins) in colorectal cancer cell lines.
Results indicate 15-lipoxygenase modified LDL as a new inducer for LOX-1 (show OLR1 Proteins) expression and as a new ligand for LOX-1 (show OLR1 Proteins).
upregulation of ALOX15 occurring in response to oxidative stress in germ cells of the male mouse leads to enhanced 4-hydroxynonenal production and subsequent pathways of deleterious protein modification
The data provide the first evidence to date that small molecules that target 12/15-LOX can prevent progression of beta-cell dysfunction and glycemic deterioration in models of type 1 diabetes.
Findings suggest a pivotal role for 12/15-lipoxygenase (12/15-LOX) in both caspase (show CASP3 Proteins)-dependent and caspase (show CASP3 Proteins)-independent apoptotic pathways following global cerebral ischemia and suggest a novel therapeutic approach to reduce brain injury following cardiac arrest.
The present study investigated the roles of arachidonate 15-lipoxygenase (Alox15) in the clearance of dying adipocytes by adipose tissue macrophages.
data support that endothelial, rather than monocytic/macrophagic, 12/15-LO has a critical role in hyperglycemia-induced ICAM-1 (show ICAM1 Proteins) expression, leukocyte adhesion, and subsequent local retinal barrier dysfunction.
This study determined that 1) deletion of 12/15-lipoxygenase (LOX) promotes the generation of epoxyeicosatrienoic acids, the cytochrome P-450-derived metabolites in postmyocardial infarction (post-MI) healing; 2) acute exposure of fatty acids to 12/15-LOX(-/-) mice drives leukocyte (neutrophils and macrophages) clearance post-MI; and 3) metabolic transformation of fats is the significant contributor in leukocyte clearance
These data suggest that systemic inactivation of the Alox15 gene normalizes the reduced fertility of male Sec46Ala-Gpx4(+/-) mice by improving the motility of their sperm. If these data can be confirmed in humans, ALOX15 inhibitors might counteract male infertility related to GPX4 deficiency.
The 12/15-LOX plays an important role in the metabolism of eicosanoids in response to allergen-induced airway inflammation.
12/15-LO-derived oxidized lipids regulate histone modifications associated with profibrotic gene expression in MCs (show SMCP Proteins), and 12/15-LO can mediate similar actions of TGF-beta1 (show TGFB1 Proteins) and diabetes.
In experimental postoperative ileus, 12/15-lipoxygenase was expressed, mainly in CX3CR1 (show CX3CR1 Proteins)(+)/Ly6C(+) infiltrating monocytes, not Ly6G(+) neutrophils. 12/15-LOX mediates ileus resolution by producing proresolving docosahexaenoic acid-derived protectin (show CD59 Proteins) DX.
demonstrates 12-lipoxygenase and some 15-lipoxygenase enzyme activity
, Arachidonate 15-lipoxygenase
, arachidonate 12-lipoxygenase, 12S-type
, arachidonate omega-6 lipoxygenase
, erythroid cell-specific 15-lipoxygenase
, omega-6 lipoxygenase
, arachidonate 12-lipoxygenase, leukocyte-type