Ask about this productRelated genes to: CYP51A1 Blocking Peptide
- Gene:
- CYP51A1 NIH gene
- Name:
- cytochrome P450 family 51 subfamily A member 1
- Previous symbol:
- CYP51
- Synonyms:
- CP51, CYPL1, P450L1, LDM, P450-14DM
- Chromosome:
- 7q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2018-02-28
Related products to: CYP51A1 Blocking Peptide
Related articles to: CYP51A1 Blocking Peptide
- Independent studies have reported that interferon-β (IFN-β) induces CYP51A1 downregulation leading to lanosterol accumulation; that lanosterol triggers HMG-CoA reductase (HMGCR) downregulation; and that statin-mediated HMGCR inhibition suppresses mast cell activation. Building on these findings, we investigated whether the known mast cell-stabilizing effect of IFN-α/β is driven by this lanosterol-induced HMGCR downregulation. In bone marrow-derived mast cells (BMMCs), IFN-α indeed induced HMGCR downregulation via both ubiquitin-mediated protein degradation and transcriptional suppression, alongside CYP51A1 downregulation and lanosterol accumulation. Co-treatment with terbinafine, a squalene epoxidase inhibitor used to prevent lanosterol synthesis, restored HMGCR expression to control levels and resulted in full recovery of BMMC function. Co-treatment with specific intermediates of the mevalonate pathway (i.e., mevalonolactone, farnesol, and geranylgeraniol) also counteracted the mast cell-stabilizing effect of IFN-α, without altering the HMGCR and CYP51A1 expression levels. These results indicate that attenuating the MVA pathway via lanosterol-induced HMGCR downregulation is directly responsible for the observed IFN-α-induced mast cell stabilization. Notably, IFN-α compromised the cortical actin dynamics necessary for FcεRI-induced LAT-PLC-γ1 signalosome assembly. These dynamics and signalosome assembly were also fully restored by co-treatment with terbinafine or the MVA pathway intermediates, as well as by the F-actin-destabilizing agent cytochalasin D. These findings were validated in vivo using a mouse model of passive cutaneous anaphylaxis and ex vivo mast cell degranulation assays. Together, our study reveals a previously unrecognized mechanism of immune regulation in which IFN-α stabilizes mast cells by impairing cortical actin dynamics through the CYP51A1-lanosterol-HMGCR axis. - Source: PubMed
Publication date: 2026/05/16
Naskar RemaYe LiuKaran SanuHong Kwan SooYeom YoungilHwang Inkyu - Colorectal cancer (CRC) incidence and mortality rates are steadily on the rise, which brings significant public health concern worldwide, especially in China. Methyltransferase-like 7 A (METTL7A), a member of the methyltransferase-like family, is associated with various cancers including CRC. Notably, CRC progression is closely linked to metabolic reprogramming. However, its precise role in CRC, particularly metabolic reprogramming of CRC, remains unclear. - Source: PubMed
Publication date: 2026/04/20
Li ShaChi XiangyinLi XiaoxueLi WanYang HongCao WanxinZhao YuxuanZhang XuMeng RuiDu GuanhuaZhang DanWang Jinhua - Enteric methane emissions from ruminants represent a significant contributor to agricultural greenhouse gases, necessitating precise genetic tools to guide mitigation strategies. This study aimed to identify genomic regions and estimate heritability parameters associated with methane-related traits in cattle through an integrated meta-analytical framework. The meta-analysis of the genome-wide association studies (meta-GWAS) was carried out with the METAL software, combining SNP level data extracted from published studies. Simultaneously, a distinct random effects meta-analysis of genomic and pedigree-based heritability estimates was performed using Comprehensive Meta-Analysis software. Functional analysis of the post-GWAS, including: Gene Ontology, KEGG, and network-based enrichment analysis, was also performed to describe the biological context of significant genes. The meta-GWAS identified 74 significant SNPs that were significant for the traits of methane, which are related to 113 candidate genes. Functional enrichment analyses revealed pathways related to metabolism, immune response, ion transport, and host-microbiome interactions. The KEGG metabolic pathway emerged as a highly enriched term, encompassing key genes such as: ALDH7A1, CYP51A1, P4HA2, and SHPK, which are involved in amino acid catabolism, lipid processing, and redox regulation functions critical to energy balance and digestive efficiency. Network analysis with Cytoscape has revealed TRPV3, TRPV1, ANK3, PKD2 and SHPK as network hub genes. Heritability meta-analysis indicated that methane production exhibited the moderate genomic (h2 = 0.296) and pedigree-based (h2 = 0.299) heritability estimations, and methane yield was also found to have moderate and high heritability. The findings highlight the potential for methane-related traits as viable targets for genetic selection. This research demonstrates the value of integrating functional genomics and quantitative genetic approaches to enhance understanding of the biological and heritable components of methane emissions, providing a robust foundation for an environmentally sustainable livestock breeding program. - Source: PubMed
Publication date: 2026/04/10
Golpasand SareGhavi Hossein-Zadeh NavidGhovvati Shahrokh - Post-stroke depression (PSD), a prevalent neuropsychiatric complication of stroke, manifests as persistent low mood and depressive symptoms secondary to cerebrovascular injury, contributing to increased morbidity and mortality. Although the modified Jie-Yu-He-Huan (MJYHH) capsule has demonstrated clinical efficacy in alleviating PSD symptoms, its pharmacological targets and mechanisms of action remain unclear. - Source: PubMed
Publication date: 2026/02/04
Wang XinyuGao QianLiu ChaoHu MinghuiLiu ZhiyaoLi ZifaZhang HaoWu LidanChen KaiXu KaiyongGeng XiwenLiu WeiWei Sheng - Glioblastoma (GBM) is a highly aggressive and therapy-resistant brain tumor, necessitating innovative multi-target strategies. Natural compounds like the triterpenoid Alisol B from Alisma orientale hold promise due to their polypharmacological potential, yet their system-level mechanisms are unclear. Using an integrated multi-omics approach (transcriptomics, proteomics, lysine acetyl-proteomics) in resistant GBM cells and validating findings in vitro and in AB strain zebrafish () xenografts, we found that Alisol B induces endoplasmic reticulum stress and G2/M arrest, initiated by extensive lysine acetylation reprogramming on histones and metabolic enzymes (e.g., FASN, FDFT1). This epigenetic rewiring leads to disrupted cholesterol biosynthesis, characterized by transcriptional activation of the mevalonate pathway alongside post-transcriptional suppression of terminal enzymes (DHCR7, CYP51A1), suggestive of toxic intermediate accumulation. Alisol B also downregulated the oncogenic axis (BIRC5-FOXM1-ITGA4) and SCD5. This study delineates Alisol B's novel multi-mechanistic action through concurrent epigenetic rewiring, metabolic dysfunction induction, and survival network dismantling. Our work elucidates the molecular pharmacology of a natural compound and provides a framework for developing polypharmacological therapies against resistant cancers, exemplifying natural products as tools to reveal new therapeutic paradigms. - Source: PubMed
Publication date: 2026/02/25
Zhang YaminShen BingfangZhang ChaoqunLi ZitingLi LishaXu XiaomeiLi HongweiLin Wenjin