Ask about this productRelated genes to: NQO2 antibody
- Gene:
- NQO2 NIH gene
- Name:
- N-ribosyldihydronicotinamide:quinone reductase 2
- Previous symbol:
- NMOR2
- Synonyms:
- QR2, DHQV, DIA6
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2017-01-27
Related products to: NQO2 antibody
Related articles to: NQO2 antibody
- Persistently infected (PI) calves resulting from maternal Bovine viral diarrhea virus (BVDV) infection during early gestation are the main source of viral transmission and pose a serious threat to the sustainable production of herds. PI cattle appear clinically normal, elucidating the molecular-level alterations is critical for understanding their specific characteristics. Moreover, the identification of candidate biomarkers for diagnosing PI cattle will provide valuable insights to support effective strategies for the control and eventual eradication of BVDV. At the same time, few studies have focused on the mothers of PI calves (Trojan dam). - Source: PubMed
Publication date: 2026/03/10
Wang JiahaoChen SiqianLai WanyiFeng XiaoZhao QingyaoMi SiyuanXu ChuangQin TongCao JieYu Ying - This study investigates the relationship between NQO1 and NQO2 gene polymorphisms and methamphetamine-associated psychosis (MAP) in the Makassar population. - Source: PubMed
Publication date: 2026/02/01
Ludong Dani HaryantoSupartını TriIsmaıl Ismail - Aflatoxin B1 (AFB1), a known mycotoxin and environmental hazard, has been linked to breast cancer, yet the exact biological pathways remain poorly characterized. We performed a comprehensive multi-omics assessment to investigate how AFB1 may influence breast tumor biology. This encompassed transcriptomic analysis, co-expression network modeling (WGCNA), immune landscape profiling, transcription factor regulatory mapping, and spatial plus single-cell transcriptomics. Predictive biomarkers were determined through a machine learning pipeline. Twenty-two genes were identified at the intersection of AFB1-predicted targets and disease-associated expression modules. A refined panel of seven biomarkers (EGFR, MIF, MET, PPARG, MME, NQO2, NR3C2) was established through model optimization. A composite classifier using glmBoost and StepGLM achieved high discriminative accuracy (area under the curve = 0.996). SHAP interpretability indicated PPARG may act protectively, while MIF showed risk-promoting characteristics. Expression heterogeneity was observed across cell populations and spatial regions. Our integrated analytical framework offers new insights into the oncogenic potential of AFB1 in breast cancer. The identified gene set may serve as both mechanistic mediators and diagnostic markers, underscoring the value of multi-omics and machine learning approaches in environmental carcinogenesis research. - Source: PubMed
Publication date: 2026/02/13
Wang WenjingLiu MengtingLi Xiang - Melatonin, an indolic neuromodulator with putative oncostatic and proposed anti-inflammatory properties, primarily demonstrated in preclinical models, is produced at extrapineal sites-most notably in the gut. Its canonical actions are mediated by high-affinity GPCRs (MT1/MT2) and by NQO2, a cytosolic enzyme with a melatonin-binding site (historically termed "MT3"). A growing body of work highlights a bidirectional interaction between the gut microbiota and host melatonin. We integrated two lines of work: (i) three clinical cohorts-cardiac arrhythmias ( = 111; 46-75 y), epilepsy ( = 77; 20-59 y), and stage III-IV solid cancers (25-79 y)-profiled with stool 16S rRNA sequencing, SCFA measurements, and circulating melatonin/urinary 6-sulfatoxymelatonin and (ii) an age-spanning cognitive cohort with melatonin phenotyping, microbiome analyses, and exploratory immune/metabolite readouts, including a novel observation of melatonin binding on bacterial membranes. Across all three disease cohorts, we observed moderate-to-severe dysbiosis, with reduced alpha-diversity and shifted beta-structure. The core dysbiosis implicated tryptophan-active taxa (Bacteroides/Clostridiales proteolysis and indolic conversions) and depletion of SCFA-forward commensals (e.g., , , , and several / spp.). Synthesised literature indicates that typical human gut commensals rarely secrete measurable melatonin in vitro; rather, their metabolites (SCFAs, lactate, and tryptophan derivatives) regulate host enterochromaffin serotonin/melatonin production. In arrhythmia models, dysbiosis, bile-acid remodelling, and autonomic/inflammatory tone align with melatonin-sensitive antiarrhythmic effects. Epilepsy exhibits circadian seizure patterns and tryptophan-metabolite signatures, with modest and heterogeneous responses to add-on melatonin. Cancer cohorts show broader dysbiosis consistent with melatonin's oncostatic actions. In the cognitive cohort, the absence of dysbiosis tracked with preserved learning across ages, and exploratory immunohistochemistry suggested melatonin-binding sites on bacterial membranes in ~15-17% of samples. A unifying microbiota-tryptophan-melatonin axis plausibly integrates circadian, electrophysiologic, and immune-oncologic phenotypes. Practical levers include fiber-rich diets (to drive SCFAs), light hygiene, and time-aware therapy, with indication-specific use of melatonin. Our conclusions regarding microbiota-melatonin crosstalk rely primarily on local paracrine effects within the gut mucosa (where melatonin concentrations are 10-400× plasma levels), whereas systemic chronotherapy conclusions depend on circulating melatonin amplitude and phase. This original research article presents primary data from four prospectively enrolled clinical cohorts (total = 577). - Source: PubMed
Publication date: 2026/01/29
Tavartkiladze AlexandreReiter Russel JLou RuiteKasradze DinaraOkrostsvaridze NanaRevazishvili PatiMaisuradze MaiaDundua GeorgeAndronikashvili IrineNozadze PirdaraJinchveladze DavidTavartkiladze LevanKhutsishvili RusudanPotskhoraia Tatia - Cervical cancer is highly prevalent in India, with most cases being diagnosed at advanced stages. Despite the standard concurrent chemoradiotherapy (CCRT), 30-40% of patients' experience treatment failure, underscoring the need for improved therapeutic strategies. Understanding resistance mechanisms and identifying predictive biomarkers are crucial to improve treatment efficacy and enable personalized medicine. We conducted a comprehensive genomic and proteomic analysis to identify molecular signatures associated with CCRT. We identified recurrent mutations in phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA) and histone-lysine N-methyltransferase 2D (KMT2D), with mutation signature analysis revealing a prevalent DNA dC- > dU-editing enzyme, APOBEC mutagenesis signature. Distinct genomic alterations, including epidermal growth factor receptor (EGFR) amplification and serine/threonine kinase 11 (STK11) deletion, were exclusively observed in the chemoradiation-resistant cohort. Proteomic analysis identified 73 significantly dysregulated proteins, with syntaxin-3 (STX3), SERPINB7, lipopolysaccharide-binding protein (LBP), EMILIN2, and ribosyldihydronicotinamide dehydrogenase (quinone) (NQO2) being the top five upregulated proteins. Integrative pathway analysis highlighted an active DNA repair pathway in the resistant cohort. This study presents the first proteogenomic profiling of cervical cancer in the Indian population, linking molecular alterations to CCRT response. STK11 and STX3 emerged as predictive biomarkers for poor response, whereas EGFR presents as a promising therapeutic target in the resistant group. - Source: PubMed
Publication date: 2026/01/26
Sambath JananiGeorge Irene AManda Srikanth SAriyannur PrasanthDhawale Ekta RKommu Raja SekharDatar RajanPatil DarshanaTrivedi VinitaSingh ManishaPrabhash KumarLimaye SewantiChauhan RichaKumar Prashant