Ask about this productRelated genes to: CYP1A1 antibody
- Gene:
- CYP1A1 NIH gene
- Name:
- cytochrome P450 family 1 subfamily A member 1
- Previous symbol:
- CYP1
- Synonyms:
- P450DX, P1-450, P450-C, CP11
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: CYP1A1 antibody
Related articles to: CYP1A1 antibody
- Clozapine is indispensable for treatment-resistant schizophrenia, but its effects on endothelial repair and their potential relevance to coronary artery disease remain insufficiently characterized. We combined a propensity score-matched nationwide cohort of 28,802 patients with experiments in primary human endothelial progenitor cells and Tg(fli1:EGFP) zebrafish embryos. Clozapine use was associated with a higher incidence of coronary artery disease during up to 12 years of follow-up (adjusted hazard ratio 1.24, 95% confidence interval 1.13-1.36). In primary human endothelial progenitor cells, clozapine was tested at 1-30 μM for 24-48 h. It concentration-dependently reduced cell growth, migration, tube formation, oxygen consumption, and extracellular acidification. In silico docking predicted a potential interaction with the aryl hydrocarbon receptor (AHR) ligand-binding pocket. Clozapine increased CYP1A1 mRNA expression and reduced AHR protein level. The AHR antagonist CH-223191 (10 μM) partially restored cell growth and shifted extracellular acidification toward control levels, supporting involvement of AHR signaling. Clozapine also increased autophagosome accumulation and LC3-II abundance, while 3-methyladenine intensified growth inhibition, consistent with a potentially compensatory autophagy-associated response. Tg(fli1:EGFP) zebrafish embryos exposed to clozapine (15 or 30 μM) during 12-30 or 30-72 h post-fertilization developed concentration-dependent vascular abnormalities and increased mortality. These findings identify AHR-associated metabolic and angiogenic dysfunction as a plausible vascular effect of clozapine, while further studies are required to determine its contribution to the clinical association and its relevance to chronic therapeutic exposure. - Source: PubMed
Publication date: 2026/09/19
Chen ChiKao Yung-ShuoTang Chih-HsinYu Chen-LinHuang Kai-YaoYen Juei-YuLin Cheng-YungHuang Chen-ChenCho Der-YangChou Meng-ChiaoWu Yi-ChengWeng Shun-LongWang Shih-Wei - Accurate interpretation of gene expression in organisms exposed to emerging contaminants (ECs) requires reliable normalization using stable reference genes. In this study, six candidate housekeeping genes (EEF1A1, GAPDH, ACTB, TBP, RAG1, and PKM) were evaluated in fish (Labeo catla) liver under exposure to chlorpyrifos, triclosan, and oxytetracycline. Expression stability was assessed using geNorm, NormFinder, BestKeeper, and the ΔC method, with RefFinder providing an integrated ranking. EEF1A1 consistently showed the highest stability, whereas PKM and RAG1 were the least reliable. Normalization of the xenobiotic response gene CYP1A1 with stable (EEF1A1) versus unstable (PKM, RAG1) genes revealed that inappropriate reference gene choice produced misleading expression profiles. These results highlight the critical importance of empirical reference gene validation for accurate qRT-PCR-based gene expression analysis, particularly in ecotoxicological studies involving exposure to complex mixtures of contaminants. - Source: PubMed
Publication date: 2026/09/18
Kumari KavitaAftabuddin MdNag Subir KumarSarkar Soma DasGhosh ShubhadeepDas Basanta Kumar - We introduce 6-methoxy-2-naphthoic acid (MONA) as a novel fluorogenic substrate for the drug-metabolizing CYP1A2 enzyme. Oxidative demethylation of MONA by human liver microsomes resulted in a red shift and a significant increase in its fluorescence. Screening 14 recombinant human cytochrome P450 (P450) enzymes revealed detectable activity in MONA demethylation by CYP1A2 (k = 12 ± 2 min, K = 578 ± 106 μM), CYP2A6 (k = 0.42 ± 0.09 min, K = 48 ± 15 μM), and CYP1A1 (k = 0.19 ± 0.09 min, K = 89 ± 43 μM). The high rate of CYP1A2-catalyzed reaction along with a distinct resolution of its K value establishes MONA as a selective fluorogenic probe for CYP1A2 activity. MONA was used to investigate the effects of chronic alcohol exposure on CYP1A2 activity using a series of 23 proteomically characterized human liver microsomes from donors with various levels of alcohol consumption. Global kinetic analysis of the set of saturation profiles yielded 2 Michaelis-Menten components with K values of 11 and 553 μM, whose combinations adequately approximate all profiles in the dataset. The amplitudes (V) of both components showed a marked increase with increasing alcohol exposure. The V of the minor high-affinity component was best correlated with a combination of abundances of CYP2E1, CYP2A6, and NADPH-P450 reductase, suggesting that it reflects the activity of CYP2A6 in the complex with CYP2E1. The V of the predominant CYP1A2-dependent component exhibits a pronounced correlation with the content of NADPH-P450 reductase, whose increased expression in alcohol consumers appears to be the main causative factor in alcohol-induced increase in CYP1A2 activity that takes place despite an alcohol-induced decrease in CYP1A2 expression. SIGNIFICANCE STATEMENT: We introduced 6-methoxy-2-naphthoic acid as a specific fluorogenic substrate for CYP1A2. By studying its metabolism in a series of 23 proteomically characterized human liver microsome samples from donors with various levels of alcohol consumption, we demonstrated a significant increase in CYP1A2 activity with increasing alcohol exposure despite decreased CYP1A2 expression. This increase, which is best correlated with the alcohol-induced increase in the abundance of NADPH-cytochrome P450 reductase, may have a striking effect on the pharmacokinetics of CYP1A2-metabolized antidepressants and antipsychotics in alcoholics. - Source: PubMed
Publication date: 2026/08/26
Gaither Kari ADavydova Nadezhda YPonraj KannapiranSingh Dilip KumarPrasad BhagwatDavydov Dmitri R - Cellular senescence is a core pathogenic mechanism of chronic obstructive pulmonary disease (COPD), and cigarette smoke (CS) acts as its primary risk factor. However, the molecular cascade linking CS exposure to pulmonary cellular senescence remains poorly defined. The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor triggered by CS-derived chemicals, has an unclarified function in smoke-induced lung cell senescence. This study aimed to verify whether AhR mediates CS-elicited pulmonary senescence through regulating oxidative stress and autophagy, and to elucidate the complete downstream signaling cascade. - Source: PubMed
Publication date: 2026/09/09
Shi Bao-YuHu Xu-DongLiu Yuan-ChengHu Si-MingZhang Guo-Xing - This study employs a multiomics approach to investigate the protective effects of fucoxanthin (Fu) and explore its potential association with metabolic and signaling pathways in diabetic mice induced by a high-fat diet combined with streptozotocin (STZ) administration. Diabetic model mice were randomly divided into normal control (NC), diabetic model, low-dose Fu (50 mg/kg/day), and high-dose Fu (100 mg/kg/day) groups. After 6 weeks of intervention, Fu treatment was associated with dose-dependent improvements in glucose and lipid metabolism, reduced oxidative stress, decreased expression of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and IL-1β) and renal fibrosis markers (TGF-β1, α-SMA, and Col1a1), along with notable attenuation of renal pathological damage. Exploratory analyses indicated that these phenotypic improvements were accompanied by reduced renal IDO1 expression, favorable shifts in tryptophan (Trp) metabolism, and upregulated AhR/CYP1A1 signaling. 16S rRNA sequencing revealed that Fu treatment was associated with a restoration of diabetes-altered gut microbiota β-diversity. Serum metabolomics identified that Fu administration correlated with alterations in multiple metabolites (including 5'-S-methyl-5'-thioadenosine, LPC 16:0, and bile acids), which are linked to key pathways such as Trp metabolism and bile acid biosynthesis. Network pharmacology predictions further suggested potential multitarget interactions of Fu with the PI3K-Akt and AGE-RAGE signaling pathways. Collectively, these findings indicate that Fu exerts potential renoprotective effects in diabetic mice, which are accompanied by a normalization of Trp-AhR pathway-related metabolism and concurrent attenuation of inflammatory, oxidative, and fibrotic responses. While causal functional links remain to be fully elucidated, these observations provide a preliminary basis for further mechanistic investigation and support the potential of Fu as a dietary supplement or adjunctive strategy for diabetic kidney disease (DKD). - Source: PubMed
Guo DonglinXie JiayongDong XueyunXu HaoXie YunhanLiu XinyuXu LinlinAli AsmaaChen MinZhang LeileiHe JiayuanWu LiangShao Keke