Ask about this productRelated genes to: CYP2W1 Blocking Peptide
- Gene:
- CYP2W1 NIH gene
- Name:
- cytochrome P450 family 2 subfamily W member 1
- Previous symbol:
- -
- Synonyms:
- FLJ20359, MGC34287
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-05
- Date modifiied:
- 2015-12-09
Related products to: CYP2W1 Blocking Peptide
Related articles to: CYP2W1 Blocking Peptide
- Aflatoxin B1 (AFB1) induces hepatocellular damage through its metabolite aflatoxin B1-8,9-epoxide (AFBO), which is produced in endoplasmic reticulum (ER) via cytochrome P450 (CYP450) enzymes. To investigate the effect of ferulic acid (FA) on AFB1-induced broiler liver damage, one-day-old Arbor Acres broilers were exposed to AFB1 (4 mg/kg) and treated with different doses of FA (60 mg/kg, 120 mg/kg, and 240 mg/kg) continuously for 28 days. The production performance, biochemical indicators, morphological changes, CYP450 enzymes' expression in ER, interactions between small molecules and CYP450 enzymes, and CYP450 enzymes' protein secondary structure were investigated. The results showed the following: (I) FA promoted broiler growth and reduced AFBO production. (II) AFB1-induced changes in serological indicators (AST, ALT, ALP, γ-GT, TBA, TG) and biochemical parameters (GST, SOD, MDA, ROS), which were reversed by FA. (III) AFB1-induced liver morphological changes and apoptosis were obviously alleviated by FA. (IV) AFB1-induced up-regulation of CYP1A5, CYP2A6, CYP2W1, and CYP3A4 in ER were reduced by FA. (V) The binding affinity of FA to CYP1A5 is lower than that of AFB1 to CYP1A5, and the binding affinity of FA to CYP2W1 is similar to that of AFB1 to CYP2W1. (VI) The contents of α helix, β sheet, β turn, and random coil in chicken CYP1A5 were 59.6%, 7.8%, 13.6%, and 19.0% respectively, and those in chicken CYP2W1 were 32.2%, 17.1%, 16.8%, and 33.9% respectively. In conclusion, FA can promote broiler growth and alleviate AFB1-induced hepatotoxicity via inhibiting and conjugating CYP450 enzymes, thus reducing AFBO formation and oxidative damage. - Source: PubMed
Publication date: 2026/05/14
Wang XingheLi WeiweiDai JiananJia MengNa LingfangXu WenyangWu ChangdeLiu Mingchun - Crustaceans, such as shrimp and crabs, are pivotal to global aquaculture, yet their productivity is severely impacted by low-temperature stress. This study employs comparative transcriptomic and genomic analyses to elucidate the molecular mechanisms underlying crustacean responses to cold stress across five economically significant species: , , , , and . We identified 4711 conserved orthogroups and analyzed differential gene expression under low-temperature conditions. Results revealed species-specific responses, with 25 orthogroups shared across all five species and 113 orthogroups common to at least four species. Functional enrichment highlighted pathways such as oxidation-reduction, hormone metabolism, immune regulation, and spliceosomes. Key genes, including , , , and , were implicated in signaling, metabolic, immunological, and developmental adaptations. Phylogenetic analysis was used to trace the evolutionary origins of stress-responsive genes, enabling the identification of both ancient conserved genes and lineage-specific genes. The results indicated that "younger" genes tend to exhibit greater transcriptional plasticity than ancient conserved genes. These findings provide critical insights into shared and species-specific low-temperature adaptation mechanisms, offering a foundation for breeding cold-tolerant crustacea strains to enhance aquaculture resilience. - Source: PubMed
Publication date: 2026/05/12
Chen YingYan WeihuaXu TongXu ShengyuZeng QifanQu ZheBao ZhenminWang Hao - Cytochrome P450 (CYP450) enzymes are essential for drug metabolism, xenobiotic detoxification, and procarcinogen activation, playing a pivotal role in both normal physiology and cancer biology. Their expression varies significantly across tissues and tumour types, reflecting the metabolic heterogeneity of cancers. Understanding these variations is critical for developing targeted therapies, optimizing drug efficacy, and minimizing toxicity. This study aimed to comprehensively profile CYP450 expression across colorectal cancer (CRC), head and neck squamous cell carcinoma (HNSCC), breast cancer, and hepatic cancer models using proteomic techniques. - Source: PubMed
Publication date: 2025/10/31
Shaheed Sadr UlAl-Eidan Ahood APors KlausPatterson LaurenceSutton Chris W - Although significant advances in the treatment of breast cancer have been made over the last few decades, searching for more effective prophylaxis and therapy for this type of cancer is still topical. Orphan cytochromes (CYPs) P450 are enzymes whose functions and substrates are not fully known. The overexpression of some orphan CYPs in breast cancer tissue warrants attention as a possible breast cancer prophylaxis/treatment target or biomarker. Of particular interest is CYP4Z1, which seems to be specific for breast cancer, including triple-negative breast cancer (TNBC). The currently available data indicate that inhibition of CYP4Z1 breast-specific expression may reduce the growth, progression, angiogenesis, and invasiveness of breast cancer. Although less specific, the other orphan CYPs, such as CYP2W1, CYP2S1, CYP2U1, and CYP4X1, exhibit significantly higher expression in breast tumors compared to normal tissues. The available data indicate that these CYP isoforms catalyze the hydroxylation of fatty acids. Their products, such as epoxyeicosatrienoic acids (EETs) or hydroxyeicosatetraenoic acids (HETEs), are considered critical modulators of cancer progression. Therefore, inhibition of the expression and activity of these orphan CYPs might be more useful in cancer treatment than in prophylaxis. This review summarizes current knowledge of orphan CYPs in breast tissue and their possible application in drug targeting or prognosis assessment. - Source: PubMed
Publication date: 2025/08/25
Licznerska BarbaraSzaefer HannaBaer-Dubowska Wanda - CNS embryonal tumors with PLAGL amplification (ET, PLAGL) are a recently described tumor type marked by amplification of one of the PLAG family genes, PLAGL1 or PLAGL2. Separately, a supratentorial, ependymoma-like CNS tumor type with PLAG family alteration, namely PLAGL1 fusion, was also reported (NET_PLAGL1). Here, we use DNA methylation profiling in combination with copy number, RNA-seq, and histological analysis to characterize and classify a novel group of CNS embryonal tumors harboring PLAG1 gene fusions (n=12). Through our screening, we identified a subset of CNS tumors (n=12) epigenetically distinct from other known CNS tumor types, but clustering close to the PLAGL1- and PLAGL2-amplified ET, PLAGL subtypes in our t-SNE analysis. Copy number profiles indicated putative PLAG1 fusions, which were confirmed in 9/12 tumors (not determined in 3/12). Different 5' fusion partners (ASAP1, ADGRG1, TMEM68, TCF4, CHD7, NCALD, HNRNPK, LOC105378102) were identified that upregulate wild-type PLAG1 through promoter hijacking. Expression analysis shows upregulation of PLAG1 as well as IGF2, DLK1, Desmin, CYP2W1, and RET, which are also robustly expressed in PLAGL1/2-amplified tumors. Patient characteristics, survival data, and clinical/imaging analysis show additional similarities to PLAGL1/2-amplified tumors. Median age at diagnosis was 5 years, tumors were located throughout the neuroaxis, and original histological diagnoses were heterogeneous. The tumors demonstrated morphologic heterogeneity, with most composed of densely cellular areas of primitive small blue cells, alongside focal regions showing clear cell morphology, microcystic changes, and ependymoma-like perivascular pseudorosettes. Applied treatment regimens were also heterogeneous, but some favorable responses to therapy were observed. In summary, we describe a third subtype of PLAG family-altered pediatric CNS embryonal tumor characterized by PLAG1 gene fusion, which leads to upregulation of PLAG1 and downstream genes. We therefore propose to rename ET, PLAGL to ET, PLAG (CNS embryonal tumor with PLAG family gene alteration) together with a specification of the respective subtype. - Source: PubMed
Publication date: 2025/08/02
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