Human ALOX15B cDNA Clone
- Known as:
- Human ALOX15B complementary Desoxyribonucleic acid Clone
- Catalog number:
- DC06852
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Human ALOX15B cDNA Clone
Related genes to: Human ALOX15B cDNA Clone
- Gene:
- ALOX15B NIH gene
- Name:
- arachidonate 15-lipoxygenase type B
- Previous symbol:
- -
- Synonyms:
- 15-LOX-2
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-22
- Date modifiied:
- 2019-01-18
Related products to: Human ALOX15B cDNA Clone
Related articles to: Human ALOX15B cDNA Clone
- Octyl (-(5-(1-indol-2-yl)-2-methoxyphenyl)sulfamoyl)carbamate has previously been characterized as substrate-specific inhibitor of the linoleic acid oxygenase activity of mammalian ALOX15 orthologs. Here we aimed at optimizing the inhibitory properties of this compound by three different chemical modifications: (i) replacement of the indole core by a phenylpyrrole; (ii) introduction of hydrophilic residues into the aliphatic hydrocarbon chain of the lead compound or by replacing this building block by a triethylene glycol moiety; (iii) replacement of the sulfamoylcarbamate group by a sulfonamide. The inhibitory potencies of the modified compounds for pure rabbit ALOX15 were quantified by in vitro inhibitory assays, and our data indicate that the replacement of the rigid indole core induced a partial loss in the inhibitor's potency. The introduction of a hydrophilic group into the aliphatic hydrocarbon chain or its replacement by a triethylene glycol moiety improved the solubility of the compound in aqueous solution, but reduced the inhibitor potency by more than one order of magnitude. Finally, the replacement of the sulfamoylcarbamate moiety by sulfonamide improved the substrate selectivity of the inhibitor for rabbit and human ALOX15. The new compounds were highly potent for human and rabbit ALOX15, but did not inhibit human ALOX15B and were less effective for mouse Alox15 (ortholog specificity). - Source: PubMed
Publication date: 2026/07/22
Gavrilyuk ViktorAksenov VladislavPetrov KirillKurchatova Angelina VBortnevskij DmitriyZhuravlev AlexanderGolovanov AlexeyKuhn HartmutIvanov Igor - Papillary thyroid carcinoma (PTC) is the most common type of primary endocrine malignancy. The tumor immune microenvironment (TIME) and genetic alterations play crucial roles in the progression of PTC. With the advance in research, there has been a heightened focus on re-evaluating molecular targeted therapies and identifying novel targets through molecular biology-based approaches. This study aimed to identify robust prognostic biomarkers and to construct a reliable risk model for patients with PTC by integrating multiomics data. - Source: PubMed
Publication date: 2026/06/26
Xu NizhenShi ZhengZheng MingjieZhang DeguangHe QiqiZhu ChuZhang ZhenleiHe GaofeiChu JunjieJiang JinxiLu XiaoxiaoCai Xiujun - Pancreatic cancer remains a devastating disease with limited therapeutic options. Accumulating evidence has shown that cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs), the predominant cells in the pancreatic cancer (PDAC) tumor microenvironment (TME), hinder anti-tumor immunity. However, the role of extracellular vesicles (EVs) in such process is poorly understood. In this study, using human bone-marrow-derived monocytes and PDAC tumor cells, we show that tumor cell-derived EVs (TC-EVs) induced monocyte differentiation towards M2-like immunosuppressive CD200R+/PD-L1+/HLA-DR- macrophages that express ALOX15b, that we identify as an independent PDAC poor-prognosis biomarker using a human pancreatic cancer metacohort. We also demonstrate that TC-EVs reprogram human primary PDAC CAFs, causing a fibronectin network reorganization associated with changes in extracellular matrix (ECM) composition, including alterations of the Wnt pathway elements such as SFRP1 enrichment. We further reveal that monocytes cultured on rSFRP1-enriched ECM differentiate also into M2-like immunosuppressive macrophages. Lastly, we demonstrate that both directly and indirectly TC-EVs, or rSFRP1-enriched ECM, driven differentiated macrophages hindered T-cell activation and subsequent anti-tumor activity. Our findings highlight novel, dual mechanisms of TC-EVs-mediated crosstalk, involving Alox15b+-Macrophages and SFRP1+-CAFs, that simultaneously contribute to foster the immunosuppressive ecosystem of pancreatic cancer. - Source: PubMed
Publication date: 2026/07/02
Hussain ZainabMontenegro ClaudioRovera ChristopherBelghoula DjamilaTubiana Sarah SimhaFinetti PascalLohmann EugenieRodrigues MagdaBertran ThomasBidaut GhislainIsnardon DanielVasseur SophieBertucci FrancoisAudebert StephaneCamoin LucRego MoacyrTomasini Richard - Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined by aberrant hepatic lipid accumulation, yet the regulatory mechanisms underlying this process remain incompletely understood. Although epitranscriptomic modifications have emerged as key regulators of hepatic lipid homeostasis, the role of N-methylguanosine (mG) modification in hepatic steatosis remains unclear. - Source: PubMed
Publication date: 2026/06/27
Li LinghuanSun YuanhaiLi LingqinZheng WanfangBian JianingLi Hanbing - Human 15-lipoxygenase-2 (h15-LOX-2), encoded by the ALOX15B gene, is a non-heme iron-containing dioxygenase implicated in the pathophysiology of atherosclerosis, cancer, and chronic inflammatory disorders through stereospecific oxygenation of arachidonic acid to 15(S)-hydroperoxyeicosatetraenoic acid, which is subsequently reduced to 15(S)-hydroxyeicosatetraenoic acid. Despite its considerable therapeutic relevance, h15-LOX-2 remains a profoundly underexplored drug target relative to its closely related isozyme, 15-lipoxygenase-1 (15-LOX-1), with which it shares only approximately 38-40% amino acid sequence identity. This fundamental sequence divergence translates into distinct active site architectures, substrate binding profiles, and tissue distribution patterns that strongly justify the pursuit of isoform-selective inhibitor development. Critically, while zileuton remains the sole clinically approved lipoxygenase-targeting drug, it is clinically used as a 5-LOX inhibitor for asthma and is not an h15-LOX-2-targeted therapy. A focused survey of the literature from 2015 to 2025 reveals that no dedicated synthetic medicinal chemistry review exclusively addressing heterocyclic scaffold-based h15-LOX-2 inhibitors currently exists. To address this gap, the present review examines synthetic heterocyclic chemotypes reported as h15-LOX-2 inhibitors or as structurally relevant 15-LOX inhibitory scaffolds, including imidazoles, thiazolidinone-thiadiazole hybrids, triazoles, quinoline-based dual inhibitors, pyrazoles, indoles, benzimidazole hybrids, xanthenones, thienopyrimidines, and isoniazid derivatives. For each scaffold class, synthetic methodologies, in vitro inhibitory potencies, structure-activity relationship analyses, isoform selectivity profiles, and computational docking findings are comprehensively discussed. Cross-scaffold analysis suggests that lipophilicity, a central heteroaromatic anchoring core capable of interacting with His373 and His378, and a geometrically constrained hydrogen-bonding feature oriented toward Ile676 may represent recurring pharmacophoric features associated with potent 15-LOX/h15-LOX-2 inhibition. Among the evaluated chemotypes, imidazole-based derivatives currently demonstrate the strongest h15-LOX-2-directed profile, with IC values as low as 0.34 μM and greater than 50-fold selectivity over related lipoxygenase and cyclooxygenase isoforms. Outstanding challenges including the scarcity of ex vivo validated compounds, species-specific translational barriers arising from divergent murine ortholog function, and the absence of wild-type inhibitor co-crystal structures are critically evaluated. Future directions encompassing covalent inhibitor strategies, PROTAC-based targeted degradation, and selective modulation of the pro-ferroptotic h15-LOX-2/PEBP1 complex are discussed as promising avenues to fully realize the therapeutic potential of this target. - Source: PubMed
Publication date: 2026/06/06
Imran Syahrul