Ask about this productRelated genes to: AHCY protein
- 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 protein
Related articles to: AHCY protein
- Metabolic cell death (MCD) modulates colorectal cancer (CRC) progression, yet its prognostic value remains unexplored. We aimed to build an MCD-centred gene signature for outcome prediction and precision therapy. - Source: PubMed
Publication date: 2026/07/16
Zhuang WeiZhang YaLiu ZhengyongYan WenxueWei TaoDeng QiupingLiu Qi - Although AHCY has been implicated in cancer progression, its specific role in endometrial cancer (EC) remains poorly understood. This study aimed to elucidate the oncogenic role of AHCY in EC and its association with patient prognosis. - Source: PubMed
Publication date: 2026/08/20
Zhang HaiyangDu LiRen WeiSun JingliPei LipengFu Yao - Intermittent fasting (IF) ameliorates metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanism remains unclear. Combined CUT&Run and transcriptomic analysis shows that hepatic Ahcy is controlled by the super‑enhancer (SE) and acts as a key mediator of IF's benefit. Liver‑specific Ahcy knockout worsens high‑fat diet (HFD)‑induced hepatic steatosis and blunts the protective effect of IF. Furthermore, inhibition of Brd4 or deletion of the core SE region reduces Ahcy expression and exacerbates lipid accumulation in vivo or in vitro. Hnf4a is identified as the transcription factor driving the Ahcy-SE. In vitro and in vivo experiments demonstrate that IF-activated Hnf4a directly binds to and activates the Ahcy-SE. Ahcy knockdown attenuates the lipid-deposition-reducing effect of Hnf4a overexpression in mice fed a HFD. In Ahcy mice, the liver SAM/SAH ratio is reduced, and Reduced Representation Bisulfite Sequencing (RRBS) and transcriptome sequencing reveal liver-specific methylation remodeling. One manifestation of this remodeling is hypermethylation of metabolic gene promoters, including the Acot12 promoter, where aberrant recruitment of Dnmt3b leads to silencing of the gene and impaired lipid hydrolysis. Therefore, these findings define an IF-Hnf4a-Ahcy pathway that activates SE-driven Ahcy to orchestrate protective epigenetic reprogramming in MASLD. - Source: PubMed
Publication date: 2026/07/27
Chen HuafengZhang ShilinDeng XiaojieXie WenqiangXu FenShen JieLiang Hua - Cardiogenic shock secondary to acute myocardial infarction (AMI-CS) prohibitively impacts survival. This prospective study aimed to discover and internally verify candidate serum protein biomarkers and evaluate their potential prognostic value for 30-day mortality in AMI-CS patients. - Source: PubMed
Publication date: 2026/07/20
Wang XiXiao Qian-FengHuang Fang-YangWang SiXu YingPu Xiao-BoYang YanChen MaoWei Xin - The methionine cycle plays critical roles in cell fate determination by shaping epigenetic landscape, yet its function in human erythropoiesis remains undefined. Here, we show that disruption of methionine metabolism by compromising the key enzyme adenosylhomocysteinase (AHCY) reshapes H3K4me3 landscape, causing erythroid cell fate reprogramming. AHCY deficiency severely impaired erythroid differentiation and expansion, leading to the generation of nonerythroid lineage hematopoietic cells, including stem/progenitor cells and immune cells, as evidenced by single-cell RNA-seq, and pseudo temporal analysis delineated a precise dedifferentiation trajectory, revealing erythroblasts transitioning back to MEPs and HSCs. Moreover, the human hematopoietic system could be reconstituted in the immunodeficient NCG-X mice by transplanting AHCY-deficient erythroblasts. Mechanistically, AHCY deficiency reduced global H3K4me3 levels and altered its genomic distribution, resulting in the upregulated expression of nonerythroid transcription factors and downregulated expression of erythrocyte lineage-specific transcription factors. Integrated single-cell analyses identified transitional states with diminished AHCY in the erythroblasts of a patient with acute myeloid leukemia (AML). Further flow cytometry confirmed the reduced H3K4me3 level in patient-derived erythroid cells. Erythroblasts isolated from patients with AML with reduced H3K4me3 exhibited a dedifferentiation potential into progenitor-like states. Our findings reveal a metabolic-epigenetic axis governing cell fate reprogramming in human erythropoiesis and provide insights into leukemia-associated anemia. - Source: PubMed
Publication date: 2026/07/14
Sun LeiZhang HengchaoLi MengjiaLin QuandeWu XiuyunCheng YingWang ShihuiHou YanWang YaomeiSheng YueLiu JingAn XiuliWang TingChen Lixiang