Ask about this productRelated genes to: AHCY Blocking Peptide
- Gene:
- AHCY NIH gene
- Name:
- adenosylhomocysteinase
- Previous symbol:
- -
- Synonyms:
- SAHH
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-05-03
Related products to: AHCY Blocking Peptide
Related articles to: AHCY Blocking Peptide
- Breast-fed (BF) and formula-fed (FF) pigs have different intestinal morphologies and physiologies. However, how molecular expression affects intestinal morphology is imperfectly known. We compare expression profiles and functions of miRNA, mRNA, and lncRNA in the intestines of 210-d-old BF and FF pigs. Jejunum and duodenum villus height and mucosal thickness were significantly higher in BF pigs than FF pigs (p < 0.05). Of 88 identified differentially expressed (DE) miRNAs in BF pigs, 39 were up- and 49 were down-regulated; of 117 lncRNAs, 53 were up- and 64 were down-regulated; and of 387 mRNAs, 242 were up- and 145 were down-regulated. GO and KEGG analysis revealed overlapping DE mRNA corresponding genes and target genes of DE miRNA and lncRNA to be associated with pathways involved in cold-induced thermogenesis, digestion, and xenobiotics metabolism. Gene families (e.g., UGT, ABC, AHCY and SLC) potentially involved in intestinal morphological development are identified. Further analysis indicates that the CYP1A1-LOC100515741/LOC100622246/LOC100739163 and AHCYL2-miR-145-3p network may regulate the development of intestinal morphology in pigs. Collectively, these results improve our understanding of the possible long-term health effects of specific alterable early-life risk factors and exposures. - Source: PubMed
Publication date: 2026/05/17
Huang YuzhiXu LanmengHuang YuluYan QingHe HangZhang Jie - As a critical rate-limiting enzyme in the methionine cycle, S-adenosylhomocysteine hydrolase (AHCY) participates in intracellular cysteine synthesis. Its overexpression has been shown to induce ferroptosis resistance in lung cancer. However, naturally derived inhibitors of AHCY remain understudied. Here, we demonstrated that AHCY overexpression attenuates the ferroptosis-promoting effect of erastin by generating homocysteine (Hcy) and glutathione (GSH) in A549 cells. Virtual screening of Traditional Chinese Medicine Active Compound Library and subsequent experimental validation identified asarinin (Ar) as a bioactive natural product that enhances the efficacy of erastin by targeting AHCY. Ar potentiates erastin-induced lipid peroxidation and ROS production by suppressing Hcy and GSH synthesis. Consistently, the ferroptosis-sensitizing effect of Ar is abolished upon supplementation with Hcy and GSH. Biochemical assays revealed that Ar exhibits high binding affinity for AHCY, inhibits AHCY activity with an IC of 22.1 µM, and increases AHCY protein stability. Molecular dynamics simulations indicated that Ar interacts with the H353 residue of AHCY. In lung cancer xenograft model, Ar alone showed minimal antitumor effects but significantly enhanced the anti-tumor activity of erastin, demonstrating promising combination therapy potential. Our findings identify Ar as a naturally derived AHCY inhibitor with potential pharmacological effects in sensitizing ferroptosis. - Source: PubMed
Publication date: 2026/05/13
Li ZiboWang YuanyuanHuang ZiyangWang ZhiyiGuo ZhenzhenXu ErpingZheng Yaqiu - Hepatic stellate cell (HSC) activation is a key driver of extracellular matrix (ECM) accumulation and liver fibrosis. Autophagy plays an essential role in regulating HSC activation, yet its metabolic regulation remains largely undefined. Curcumol, a bioactive compound derived from Curcuma longa, possesses potent antifibrotic activity, but the underlying metabolic mechanisms are unclear. In this study, we found that curcumol suppressed HSC activation and induced autophagy-dependent cell death, together with inhibition of methionine metabolism. Curcumol treatment reduced LX-2 cell viability and downregulated profibrogenic markers α-smooth muscle actin (α-SMA) and collagen type I (COL1A1) in a dose-dependent manner. Mechanistically, curcumol enhanced LC3-II accumulation, diminished p62 levels, and promoted autophagic vacuole formation, effects that were reversed by the autophagy inhibitor 3-methyladenine (3-MA). Silencing of ATG7 attenuated curcumol-induced autophagy-associated changes and cell death, supporting the involvement of ATG7 in this process. Furthermore, curcumol significantly reduced the expression of key methionine cycle enzymes MAT2A and AHCY. Supplementation with S-adenosylmethionine (SAM) partially reversed curcumol-associated changes in methionine metabolism and autophagy-related markers, and improved HSC viability, supporting a functional link between methionine metabolism and the observed phenotype. Collectively, these findings suggest that curcumol promotes autophagy-dependent death of HSCs in association with disrupted methionine metabolism, providing new insight into the metabolic basis of its antifibrotic action. - Source: PubMed
Publication date: 2026/05/08
Gao Yi-JieZhou YaLi Yi-NingYang Kai-YaoXia Si-WeiHu Meng-RuLi YangChen LiWang Fei-XiaLu ShuaiLian Na-QiZheng Shi-ZhongZhang Feng - Nasopharyngeal carcinoma (NPC) is a widely prevalent malignant tumor with a marked tendency toward metastasis and recurrence. Ferroptosis-related genes (FRGs) are critically involved in the pathogenesis of NPC. This study aims to employ bioinformatics analysis methods to identify key genes influencing the malignant progression of NPC and to investigate the regulatory mechanisms of these genes. - Source: PubMed
Publication date: 2026/02/25
Zheng HuizhenWang XiaodanChen Qin - Colorectal cancer (CRC) is a major cause of morbidity and mortality, with chronic inflammation from inflammatory bowel disease (IBD) representing a well-established risk factor. Clarifying shared molecular mechanisms may facilitate early detection and prevention strategies. - Source: PubMed
Dhami JaiyaRadhakrishnan Swarnima KollampallathRuss DominicMondal SudipAlzarooni AbdulrahmanMerodio Laura BravoDuggal Niharika AGupta RuchiAcharjee Animesh