Ask about this productRelated genes to: CYP1A1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: CYP1A1 Blocking Peptide
- Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon and environmental pollutant, has been implicated in the exacerbation of psoriasis, although the underlying molecular mechanisms remain unclear. In this study, we investigated the role of BaP in inflammation, focusing on serum exosomes, using a mouse model of imiquimod (IMQ)-induced psoriasis. Topical BaP exposure aggravated psoriatic skin inflammation and increased the expression of aryl hydrocarbon receptor (AhR), CYP1A1, and proinflammatory cytokines in lesional skin. Serum exosomes from BaP + IMQ-treated mice enhanced cytokine expression in primary mouse keratinocytes. High-throughput miRNA profiling revealed that 81 and 91 miRNAs were upregulated in serum exosomes from IMQ- and BaP + IMQ-treated mice, respectively, compared to controls. Notably, mmu-miR-423-3p was the most upregulated in both groups, as validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Consistently, hsa-miR-423-5p was significantly elevated in circulating exosomes from psoriasis patients compared to healthy controls, confirmed by miRNA sequencing and qRT-PCR. KEGG pathway analysis linked hsa-miR-423-5p to the MAPK signalling pathway. Functionally, miR-423-5p triggered an increase in the expression of pro-inflammatory cytokines and oxidative stress in psoriatic keratinocytes. These findings suggest that BaP exacerbates psoriatic inflammation via AhR signalling and that serum exosomal miR-423 may serve as a biomarker for environmentally induced psoriasis exacerbation. - Source: PubMed
Kim Hye RanPark Jin SeoKim Hye OnePark Chun WookChung Bo Young - Aiming to develop a high-throughput fluorimetric assay for the activity CYP1A2, we introduced 6-Methoxy-2-naphthoic acid (MONA) as a new fluorogenic substrate for this important metabolizer of antidepressants and psychotropic drugs in human liver. We demonstrated that oxidative demethylation of MONA by liver microsomes results in a red shift and a substantial increase in fluorescence. This effect, which is exceptionally well pronounced at alkaline pH, allowed us to develop a sensitive and robust high-throughput assay of MONA metabolism. Probing the activity of 15 individual recombinant human P450 enzymes, we found that only two P450 species exhibited activity in MONA demethylation: CYP1A2 ( =11.9±2.2 min , =578±106 µM) and CYP2A6 ( =0.48±0.07 min , =54±15 µM). Since the values of the two enzymes are well resolved and the turnover rate observed with CYP2A6 is much lower than that of CYP1A2, this new fluorogenic substrate is useful as a specific probe for CYP1A2 activity in HLM. Importantly, MONA is not metabolized by CYP1A1 and CYP2C19, which distinguishes it from all known CYP1A2 fluorogenic substrates. We then used MONA to investigate the effects of chronic alcohol exposure on CYP1A2 activity using a series of 23 proteomically characterized individual HLM preparations from donors with various levels of alcohol consumption. The substrate saturation profiles (SSP) acquired with these preparations were subjected to global kinetic analysis by approximating them with combinations of two Michaelis-Menten equations with globally optimized values of 11 and 553 µM. The amplitudes ( values) of both components showed a pronounced increase with increasing alcohol exposure of the liver donors. The of the minor high-affinity component was best correlated with the abundance of alcohol-inducible CYP2E1 enzyme. The correlation was further improved by combining it with the abundances of CYP2A6 and CPR. This finding suggests that this minor component reflects the activity of CYP2A6 in the complex with alcohol-inducible CYP2E1 protein. In contrast, the of the predominant CYP1A2-catalyzed low-affinity component revealed a pronounced correlation with the abundances of CYP1A2 and NADPH cytochrome P450 reductase (CPR). These results suggest a considerable increase in the rate of metabolism of drug substrates of CYP1A2 by chronic alcohol exposure that takes place despite an alcohol-induced decrease in CYP1A2 expression. - Source: PubMed
Publication date: 2026/02/23
Gaither KariDavydova NadezhdaPonraj KannapiranSingh Dilip KPrasad BhagwatDavydov Dmitri R - Polysaccharides derived from edible fungi can alleviate ulcerative colitis (UC) by enriching beneficial probiotics. However, the mechanisms underlying their interaction with probiotics remain unclear. Here, The current study investigated how PCP enriches L. gasseri and the effects of L. gasseri on dextran sulfate sodium (DSS)-induced UC. Genomic analyses predicted multiple polysaccharide utilization loci in L. gasseri, and growth kinetics together with gene expression assays confirmed that PCP promoted L. gasseri growth and upregulated glycoside hydrolases (GH1 and GH3). In UC induced mice, L. gasseri alleviated weight loss, colon shortening, and Disease activity index score, increased goblet cells, and decreased pro-inflammatory cytokines. In addition, targeted metabolomics revealed that L. gasseri intervention was associated with the restoration of indole-3-lactic acid (ILA) and indole-3-propionic acid (IPA) levels in the tryptophan-indole metabolic pathway. RT-qPCR, Western blot, and immunofluorescence analyses showed that L. gasseri intervention induced the upregulation of AHR expression and the downstream genes CYP1A1 and IL-22. Treatment with the AHR antagonist CH223191 further confirmed that the anti-inflammatory and barrier-protective effects were dependent on the AHR pathway. Notably, It was further verified through ABX depletion experiments that PCP exerts its indirect therapeutic effect via L. gasseri. Consequently, this study provided new insights into the interaction between PCP and probiotics the mechanism underlying the protective role of L. gasseri in the intestinal barrier, and proposes promising preliminary combination strategy for the treatment and prevention of UC. - Source: PubMed
Publication date: 2026/05/07
Zhang ChenYu LuzheLiu YingyingXu MinYu JieLiu JianZhang XianWang LeiPeng DaiyinLi SuliangWang YanyanChen WeidongZhang Yue - Cuproptosis, a newly discovered form of copper-driven regulated cell death, has been shown to be closely related to ovarian function. However, whether the oocyte dysfunction, decreased ovulation efficiency, and cumulus cell aging caused by copper overload or imbalance are associated with regulatory pathways related to cuproptosis remains unclear. In this study, the expression profiles of genes related to cuproptosis in cumulus cells were comprehensively analyzed through transcriptome sequencing and metabolome analysis, and key genes and pathways that affect oocyte maturation were identified in response to elesclomol and CuSO treatment. Transcriptome analysis of cumulus cells revealed the differential expression of genes involved in key biological processes, such as cellular senescence (AKT3, MORC3, RBL1, etc.), gap junctions (GJA1, GNAI1, GJB3, etc.), steroid biosynthesis (FDX1, HSD17B7, CYP1A1, etc.), and cell cycle regulation (CDK2, CCNB2, MAPK7, etc.). Metabolomic analysis revealed significant changes in the levels of malic acid, PS (18:3(10,12,15)-OH(9)/14:0), and PA (21:0/LTE4), among other compounds. Subsequent Smart-seq analysis of oocytes revealed that after cuproptosis was induced in cumulus cells, oocyte maturation was disrupted, which affected genes associated with cellular senescence (TGFB2, SIRT1, CHEK2, etc.), oocyte meiosis (FBXO5, CCNB3, PLK1, etc.), and DNA methylation (PPM1D, DNMT3B, KMT2A, etc.). These findings provide deeper theoretical support for the key genes and biological processes involved in cumulus cell regulation and oocyte maturation, further clarifying the regulatory mechanisms of cuproptosis in the field of reproduction. - Source: PubMed
Publication date: 2026/05/05
Xu HongTian TianXu DanDu XiaoxueSu RuiLiang JinghongLiu YingZhang YuqingLiu ChangLiang ShuangLi QingyingDing DeliHan YongshengZhai BoLi JidongChen ChengzhenZhang JiabaoJiang HaoYuan Bao - Arsenic trioxide (ATO) is both a life-saving therapy for acute promyelocytic leukemia and a systemic toxicant whose hepatic effects remain incompletely defined. This study examined how a single clinically relevant ATO dose (8 mg/kg, i.p.) acutely remodels hepatic xenobiotic-metabolizing enzymes, arsenic transporters, and pro-inflammatory mediators in male and female C57Bl/6 mice. Mice were treated with ATO or saline and livers were collected at 6 and 24 h for integrated mRNA and protein profiling of major Cytochrome P450 (CYP) families, aquaglyceroporins (), ATP-binding cassette () transporters, and cytokines (). ATO induced highly sex-, time-, and isoform-specific reprogramming. Females exhibited a wider and earlier decline in several female-predominant CYP2, CYP3, and CYP4 isoforms, including a more pronounced reduction in hepatic CYP3A, CYP4A, and CYP4F protein abundance. In contrast, males showed mainly transcriptional induction of specific genes (, , , and ), accompanied by comparatively modest decreases in overall CYP protein levels. and transporters were differentially modulated, with males displaying early, relatively monotonic upregulation of efflux systems, while females exhibited higher basal expression but more complex, biphasic regulation of both influx () and efflux pathways. These transcriptional changes paralleled a transient inflammatory response, including early induction and female-specific elevation. Collectively, these findings highlight sex-dependent modulation of hepatic ATO handling and drug metabolizing capacity, with important implications for risk assessment and individualized ATO containing regimens. - Source: PubMed
Publication date: 2026/05/08
El-Mahrouk Sara REl-Kadi Ayman O S