Ask about this productRelated genes to: CYP27A1 Blocking Peptide
- Gene:
- CYP27A1 NIH gene
- Name:
- cytochrome P450 family 27 subfamily A member 1
- Previous symbol:
- CYP27
- Synonyms:
- CTX, CP27
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-22
- Date modifiied:
- 2015-12-09
Related products to: CYP27A1 Blocking Peptide
Related articles to: CYP27A1 Blocking Peptide
- The circadian clock regulates multiple physiological processes in the skin, including local hormone synthesis and pigmentation. However, how circadian regulation interacts with epidermal endocrine signalling in melanocytes remains unclear. In this study, we investigated whether core circadian regulators influence melanogenesis in human melanocytes and explored their potential link to epidermal endocrine factors and pigmentary disease. Primary normal human epidermal melanocytes were analysed following siRNA-mediated knockdown of the core clock genes basic helix-loop-helix ARNT-like protein 1 (BMAL1) and CLOCK circadian regulator (CLOCK). Silencing either gene significantly reduced melanin synthesis and altered the expression of hormone-related factors. Notably, expression of the vitamin D-metabolizing enzyme CYP27A1 was markedly decreased after BMAL1 or CLOCK knockdown, changes that were associated with reduced melanogenic activity. Consistently, immunohistochemical analysis revealed diminished CYP27A1 expression in melanocytes within vitiligo lesions. These findings demonstrate that disruption of circadian clock regulators impairs melanogenesis and is accompanied by alterations in vitamin D-related components. Our results suggest that circadian regulation may modulate pigmentation partly through effects on vitamin D metabolism, providing new insight into the mechanisms underlying pigmentary disorders. - Source: PubMed
Zhu AnyaYang LingliLai SylviaYang FeiTsuruta DaisukeKatayama Ichiro - Comprehensive quality control is essential for ensuring the efficacy and safety of traditional Chinese medicines (TCMs). However, current quality control methods of TCMs primarily focus on quantifiable indicators, neglect the variation of pharmacodynamic constituents across disease progression. This study aimed to develop a comprehensive pathogenesis-oriented quality control framework for TCMs, using Radix ginseng-Schisandra chinensis (R-S) herb pair intervention in hepatocellular carcinoma (HCC) progression as an example. A rat model of "hepatitis-cirrhosis-HCC-advanced HCC" was established to evaluate the effects of R-S. Untargeted metabolomics revealed that bile acid (BA) dysregulation was the key pathological mechanism in HCC progression. Target metabolomics, liver-incorporated constituents analysis, immunoblotting techniques, correlation analysis and weighted average algorithm were integrated to screen the pharmacodynamic substances of R-S. HPLC fingerprinting of R-S was established and analyzed using machine learning (ML) algorithms to identify characteristic constituents. Ultimately, the Q-markers of R-S were ascertained and verified by molecular docking and molecular dynamics simulation. R-S effectively restored BA homeostasis during the progression in HCC by modulating the aberrant expression of BA-regulatory proteins (BSEP, MRP2, OATP1B1, NTCP1, CYP27A1, and CYP7A1). 6, 8, and 8 pharmacodynamic components of R-S were identified for preventing the further progression of hepatitis, cirrhosis, and HCC, respectively. Furthermore, 7 characteristic constituents of R-S were determined. Ultimately, 5 specific, measurable, and effectively Q-markers were identified. This study provides a reliable framework for facilitating precise quality control and applications of TCMs. - Source: PubMed
Publication date: 2026/06/08
Li SaiyuDong YijingGu RuiGuan LifangSong JiaqiZhang MingzheZhang QianLi QingZhang Yiwen - Craniosynostosis is defined by premature cranial suture fusion and is biologically heterogeneous. To map mitochondrial-associated signals in craniosynostosis and rank follow-up candidates, we integrated two public microarray datasets (GSE27976, GSE50796), corrected batch effects, and analyzed 14,186 shared genes using limma. This identified 798 nominal DEGs (388 upregulated and 410 downregulated), of which 19 remained significant after Benjamini-Hochberg correction. Intersecting the nominal DEG list with the MitoCarta 3.0 inventory yielded 24 mitochondrial DEGs (MitoDEGs). Complementary feature selection reduced these 24 MitoDEGs to an eight-gene panel (TMEM11, SLC25A21, GPT2, CYP27A1, MRPS30, ACAA2, GSR, and LIG3); a multigene score reached an apparent AUC of 0.806 in the integrated dataset. Correlation-based co-expression analyses linked the panel to mitochondrial translation, electron transport, amino-acid metabolism, redox control, and cell-matrix signaling. Among craniosynostosis cases, consensus clustering on the eight genes separated two molecular subtypes with distinct GSVA pathway profiles. For experimental support in a genetically defined mouse model, we profiled bilateral coronal suture complexes from Fgfr2C361Y/+ knock-in (KI) pups and WT littermates. Jess capillary immunoassay showed higher CYP27A1 abundance in KI sutures (P = 0.0276), whereas ACAA2, LIG3, MRPS30, and TMEM11 were not significant. Data-independent acquisition (DIA) proteomics identified 523 differentially abundant proteins (516 increased, 7 decreased in KI), followed by stricter-threshold reporting, sensitivity analysis, and threshold-free rank-based enrichment. MitoCarta proteins and mitochondrial pathways remained supported under these more conservative analyses. These results support mitochondria-associated transcriptomic and proteomic changes in craniosynostosis and prioritize a limited set of mitochondrial candidates for future mechanistic work. - Source: PubMed
Publication date: 2026/06/08
Zeng HanWang YuDong MiaoYue YingyingJin Xiaolei - Hepatic ischemia-reperfusion injury (IRI) is a complex event influenced by interconnected immune and metabolic processes. Steatotic livers are especially sensitive to IRI, but the crosstalk between innate inflammatory responses and lipid metabolic dysregulation in this context is not well understood. Using transcriptomic profiling in a murine high-fat diet (HFD) model, we assessed immune and metabolic responses to hepatic IRI and examined the effects of N-acetylcysteine (NAC). In steatotic livers, IRI induced the upregulation of inflammatory mediators, including TLR/NF-κB-associated genes (, , ) and neutrophil-associated genes (, ), accompanied by the downregulation of lipid and cholesterol metabolism-related genes, including , , , and . NAC supplementation attenuated inflammatory gene expression and restored key lipid biosynthetic regulators. We then performed targeted lipidomic analysis to determine whether NAC-mediated transcriptional changes were reflected at the lipid level and observed a significant increase in total phosphatidylcholine and sphingomyelin in steatotic livers following IRI. Finally, to assess the contribution of innate immune cells to hepatic IRI, we quantified neutrophils and macrophages in HFD+NAC IRI and HFD IRI livers. We found that NAC supplementation reduced hepatic neutrophil accumulation and markedly decreased LCN2 expression following IRI. - Source: PubMed
Publication date: 2026/05/19
Kang JimanPatil DigvijayHackett RyanCui YukiOza KeshaRutkowski AbigailLiggett Jedson RLi HenghongRanjit SumanKwon DongHyangKallakury BhaskarAlbanese ChrisGondolesi Gabriel EEkong UdemeCui WanxingKhan KhalidFishbein Thomas MKroemer Alexander - Age-related macular degeneration (AMD) is a leading cause of irreversible central vision loss in older adults. Neovascular AMD (nAMD) is characterized by choroidal neovascularization (CNV), vascular leakage, and fibrotic remodeling. Although anti-vascular endothelial growth factor (VEGF) therapy has improved visual outcomes for some patients, emerging findings highlight growing concerns regarding treatment resistance, persistent disease activity, and progression to subretinal fibrosis, which remain major challenges. Growing evidence indicates that nAMD arises from the interplay among metabolic dysfunction, oxidative stress, chronic inflammation, hypoxia signaling, and extracellular matrix remodeling within the outer retina. Disruption of mitochondrial function, lipid handling in the retinal pigment epithelium, complement activation, inflammasome signaling, macrophage immune-metabolic reprogramming, and hypoxia-driven VEGF expression collectively shape angiogenesis and lesion progression. Murine models, including laser-induced CNV, two-stage laser-induced fibrosis, and spontaneous or genetic systems such as JR5558, VLDLR-deficient, and CYP27A1-deficient mice, have provided essential mechanistic insights into these pathways. Aging and biological sex influence metabolism, mitochondrial efficiency, immune responses, hypoxia responsiveness, and wound-healing capacity. However, many widely used experimental models rely on young adult animals and often use a single sex without accounting for sex- or age-based differences, leaving these critical factors understudied and inadequately integrated into preclinical design. This review integrates current mechanistic understanding with a critical evaluation of murine nAMD models and emphasizes the importance of incorporating biological age and sex into experimental systems to improve mechanistic interpretation and translational relevance. - Source: PubMed
Publication date: 2026/05/29
Harris ChanelNisar Mohammad AAmamoo RonnyPatel RahulMartin Pamela MJadeja Ravirajsinh NThounaojam Menaka C