Ask about this productRelated genes to: NQO1 Blocking Peptide
- Gene:
- NQO1 NIH gene
- Name:
- NAD(P)H quinone dehydrogenase 1
- Previous symbol:
- NMOR1, DIA4
- Synonyms:
- DHQU, QR1, DTD
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-07-12
Related products to: NQO1 Blocking Peptide
Related articles to: NQO1 Blocking Peptide
- Ammonia acts as a key environmental pollutant in fish farming. Elevated ammonia concentrations can induce stress responses in fish, threatening their survival and growth. As a vital metabolic organ, the fish liver plays key roles in detoxification and immune defense. In the present study, juvenile hybrid groupers (Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂) were subjected to ammonia stress at 4 mg/L (A4) and 8 mg/L (A8) over a 7-day period. Subsequently, multiple physiological aspects of the liver were assessed across several biological levels, encompassing histomorphology, oxidative stress, inflammatory factors, and metabolic profiles. The results showed that ammonia stress caused hepatic morphological alterations and triggered oxidative stress and inflammatory responses. In detail, MDA content and T-AOC and SOD activities were increased in the A4 and A8 groups (P < 0.05), and LPO content was increased in the A8 group (P < 0.05). Meanwhile, the mRNA expression levels of nrf2, trx, tnfα, and il1β genes were upregulated in the A4 and A8 groups (P < 0.05); gpx and il8 genes were upregulated but il10 gene was downregulated in the A8 group (P < 0.05); nqo1 gene was downregulated in the A4 group (P < 0.05). Furthermore, the hepatic metabolite profiles were perturbed, particularly "histidine metabolism" and "biosynthesis of valine, leucine, and isoleucine" pathways. Additionally, several functional metabolites, including L-tryptophan, indole, carnosine, citric acid, sphingosine, pantothenic acid, and inositol, were emerged as potential candidate biomarkers. These findings demonstrated that ammonia stress could induce physiological dysfunction in the liver of groupers through a cascade of tissue damage, activated oxidative stress, disrupted inflammatory responses and altered metabolic profiles, and such adverse effects were markedly aggravated with the increase in ammonia concentration. Future research should focus on long-term ammonia exposure, concentration-time dose effects, and multi-omics integration to clarify the underlying response mechanisms. - Source: PubMed
Publication date: 2026/05/19
Fang ZhangshengWang YunZhu RuijieDuan Yafei - Dilated cardiomyopathy (DCM) is a clinically heterogeneous cardiac disorder characterized by ventricular dilation and systolic dysfunction, with limited options for mechanism-based diagnosis and targeted therapy. Programmed cell death (PCD), encompassing apoptosis, ferroptosis, pyroptosis, and other regulated mechanisms, has been implicated in the pathogenesis of DCM, yet its diagnostic and therapeutic relevance remains incompletely understood. Here, we performed an integrative multi-omics analysis combining bulk and single-cell RNA sequencing datasets to identify PCD-related molecular features associated with DCM. Through differential gene expression, WGCNA, and six machine learning algorithms, eight core genes (AGTR2, GLI2, HRK, IL10, NQO1, NT5E, SFRP1, and STAT4) were identified and used to construct a predictive model evaluated across five independent cohorts. Immune infiltration and consensus clustering revealed two distinct molecular subtypes with differential immune-metabolic signatures. Single-cell analysis demonstrated cell-type-specific expression, particularly in fibroblasts and immune cells. Drug-gene interaction mapping and molecular docking highlighted decitabine and folic acid as potential therapeutic candidates. Expression of key genes was partially validated at the mRNA and protein levels in both human and mouse myocardium. Notably, given that most transcriptomic datasets represent advanced-stage disease, these findings may reflect shared molecular features of cardiac remodeling rather than early disease-specific mechanisms. This study provides insights into PCD-associated molecular alterations in DCM and offers a basis for future research into molecular stratification and therapeutic targeting. - Source: PubMed
Publication date: 2026/05/18
Fan JiliChen LihongShang WentaoWang XiaotongGan TianTan XinSong LaichunBo Xiaohong - Emerging evidence has shown that microbiota dysbiosis and aberrant bile acid (BA) profiles are correlated with disease progression. This study elucidates dysregulated BA metabolism in psoriasis patients and imiquimod-treated female mice, coupled with increased expression of the farnesoid X receptor (FXR) in keratinocytes. Activation of FXR by glycochenodeoxycholic acis (GCDCA) ameliorates psoriatic symptoms by enhancing lipid metabolism, particularly fatty acid oxidation. Mechanistically, the FXR-mediated enhancement of antioxidant capacity by upregulating NQO1 expression underlies its regulatory role in lipid metabolism, offering an insight into FXR's role in oxidative stress and lipid metabolism. Conversely, keratinocyte-specific FXR ablation exacerbates psoriasis severity. Gut microbiota dysbiosis is further identified as a pivotal contributor to perturbations in BA profiles in psoriasis. These preclinical findings support a mechanistic model linking gut microbiota dysbiosis and BA alterations to FXR signaling in keratinocytes and psoriasis-associated metabolic dysregulation, suggesting therapeutic potential for microbiota-targeted interventions. - Source: PubMed
Publication date: 2026/05/18
Lian PanpanLu RenweiGu ChaodeWazir JunaidWang WentongZong YangyongyiXia YunNi JieChen HuimeiPetretto EnricoTreuter EckardtFan RongrongYang AirongSu ZhonglanWang HongweiHuang Zhiqiang - Myocardial ischemia/reperfusion (I/R) injury is a major challenge in reperfusion therapy for acute myocardial infarction, primarily due to excessive oxidative stress, inflammation, and cardiomyocyte apoptosis. MicroRNAs are known regulators of cellular stress responses, but the role and underlying mechanism of miR-200a-3p in myocardial I/R injury remain unclear. - Source: PubMed
Publication date: 2026/05/01
Zhao YanboLiu LuluShen XiaohuaWang MinWang MeihuiSun LinglingZhang Kai - Lung cancer with SMARCA4 deficiency has a high degree of malignancy and a low degree of differentiation. It is a newly discovered type of tumor closely related to gene mutations. The present study aimed to clarify the molecular mutation characteristics of -deficient lung cancer using next-generation sequencing (NGS). NGS sequencing was conducted to analyze the gene expression profile of 15 patients with deficient lung cancer, with positive or negative EGFR expression, and the association between gene mutation sites and expression was analyzed. The pathological characteristics of -deficient lung cancer were analyzed using immunohistochemistry. The likelihood of positivity for the programmed cell death 1 ligand 1 protein was low, and there were no instances of positivity for anaplastic lymphoma kinase protein expression. Approximately 50% of Ki67-positive expression regions were present. The BOI-related E3 ubiquitin-protein ligase 1 protein encoded by the gene was not expressed; however, the INI1 protein encoded by was partially positive (6/15), which showed that the expression of INI1 was not affected by . The mutation types included c.2729C>T (p.T910M), c.3634_3636del (p.E1212del), c.3574C>T (p.R1192C), and c.3733G>A (p.A1245T). and mutations were detected in nine patients, mutation was detected in seven patients, mutation was detected in six patients and mutation was detected in five patients. The mutated genes were more resistant to the EGFR tyrosine kinase inhibitor. In conclusion, patients with -deficient lung cancer have distinct immunohistochemical characteristics, and has been implicated in the incidence and progression of tumors through different mutation mechanisms. - Source: PubMed
Publication date: 2026/05/05
Yang FeichengYang YuzhongChen ZhihongLi YanchunSong Yinghui