AHCY Pre-design Chimera RNAi
- Known as:
- AHCY Pre-design Chimera RNAi
- Catalog number:
- H00000191-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AHCY Pre-design Chimera RNAi
Related genes to: AHCY Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: AHCY Pre-design Chimera RNAi
- As a prominent replacement for conventional perfluorooctane sulfonate (PFOS), 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA) has been widely used, raising health concerns. However, the precise toxicological impacts of this compound on the male reproductive system remain largely uncharacterized. To address this gap, we employed a comprehensive strategy integrating computational prediction, multi-omics analysis, and cell experiments to investigate potential molecular links between 6:2 Cl-PFESA exposure and non-obstructive azoospermia (NOA)-associated spermatogenic dysfunction. Among 977 putative target genes of 6:2 Cl-PFESA, 69 overlapped with NOA-associated differentially expressed genes (DEGs). Machine-learning analyses further identified DOT1L and AHCY as the most prominent candidate targets. Both genes were downregulated across independent NOA cohorts and were predominantly expressed in spermatocytes, spermatogonia, and spermatids according to single-cell transcriptomic analysis. Molecular docking suggested potential interactions between 6:2 Cl-PFESA and DOT1L or AHCY. Their expression was also associated with ssGSEA-derived enrichment scores for macrophages, regulatory T cells, and Th1 cells. In GC-1 spg cells, 6:2 Cl-PFESA exposure increased reactive oxygen species production and apoptosis and reduced DOT1L and AHCY protein levels. Overall, these findings suggest that DOT1L and AHCY may be involved in the response of spermatogonial cells to 6:2 Cl-PFESA exposure, thus providing a basis for further mechanistic investigation. - Source: PubMed
Publication date: 2026/09/28
Shi WeiZhang YingLu LuZhou QianZhang HuPu YuepuYin Lihong - Chronic cold stress disrupts hepatic metabolism and fetal development of Mongolian sheep in northern pastoral zones, while systematic nutritional mitigation strategies remain poorly characterized. N-carbamylglutamate (NCG) promotes endogenous arginine synthesis; however, its hepatic regulatory roles against cold stress in pregnant ewes and fetuses remain unclear. This study explored the potential protective effects of NCG via integrated hepatic transcriptome and metabolome analysis. Twenty-four late-gestation ewes were assigned to warm control, cold stress, and cold stress + NCG supplementation groups. Hepatic mRNA, lncRNA, circRNA, and miRNA sequencing, untargeted LC-MS metabolomics, multi-omics conjoint analysis, and qRT-PCR verification were performed using ewe and fetal liver tissues. The results indicated that cold stress potentially was associated with mTOR, PI3K/AKT, amino acid, and energy metabolic pathways, inducing extensive transcriptomic and metabolic alterations. NCG supplementation might reverse cold-induced transcriptional and metabolic disorders and restore glutathione and cysteine-methionine metabolism. qRT-PCR validated the differential expression of core hub genes AK4, AHCY, and RRM2, linking transcriptomic and metabolic reprogramming. Divergent hepatic molecular responses to NCG were observed between ewes and fetuses. Multi-omics correlation analysis suggested that maternal NCG may modulate hepatic energy and amino acid metabolism through mTOR and redox-related pathways under cold stress and potentially exert transgenerational hepatic effects on fetuses. These findings provide preliminary omics-based mechanistic hypotheses and a theoretical basis for nutritional intervention against cold stress in sheep production. - Source: PubMed
Publication date: 2026/09/18
Li KangZhi YuShi LuluTian JingLi YunhuaDu JuanZhang MeimeiZhang HaoDong ZhongWang RuijunGuo WeiyongGuo Tianlong - 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