Ask about this productRelated genes to: AS3MT Blocking Peptide
- Gene:
- AS3MT NIH gene
- Name:
- arsenite methyltransferase
- Previous symbol:
- -
- Synonyms:
- CYT19
- Chromosome:
- 10q24.32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2016-10-05
Related products to: AS3MT Blocking Peptide
Related articles to: AS3MT Blocking Peptide
- Coastal transition zones (CTZs) are dynamic zones where seawater intrusion and freshwater discharge interact. Arsenic (As) is a common contaminant in these zones, however its co-transport with increasing abundance microplastics (MPs) remains unclear. In this study, saturated column experiments combined with Hydrus-1D modeling were used to investigate the co-transport of As with polystyrene (PS), polyethylene (PE), and polylactic acid (PLA). Increasing salinity inhibited As transport in the absence of MPs. Under the same salinity, MPs generally increased As breakthrough, following the order PS > PE > PLA. With salinity increased, PS maintained a slight promoting effect on As breakthrough, whereas PE and PLA exhibited reduced breakthrough under high-salinity conditions. Co-transport was most pronounced at an As:MP ratio of 1:2, although PLA showed a non-linear response and lower As mobility at 1:1. Simulated seawater intrusion indicated that ionic-strength fluctuations produced distinct release peaks. MPs further enhanced non-equilibrium As release during flushing. Metagenomic sequencing of samples from the 21-day experiment indicated that MPs altered the microbial communities and increased the relative abundance of several As-related genes (such as AS3MT and arsC), particularly in the PS treatment. These findings clarify the effects of MPs on As transport and support risk assessment for coastal groundwater systems. - Source: PubMed
Publication date: 2026/05/14
Hua YiziXue YuanLi ZhiZhang YutingLiu QinglongLiu LinanTang Jingchun - Arsenic poisoning has severe health effects, and accordingly, most research on the arsenite methyltransferase 3 (AS3MT) enzyme has focused on its role in arsenic metabolism, overlooking potential endogenous functions. We discovered an arsenic-independent role for AS3MT in regulating hepatic energy metabolism. as3mt loss in zebrafish caused differential expression of thousands of genes in the liver, with many of the downregulated genes playing roles in mitochondrial energy metabolism. Similar genes were downregulated in AS3MT-depleted human cells. as3mt zebrafish mutants had large, malformed mitochondria, were more sensitive to both arsenic and the mitochondrial toxin rotenone, and impaired swimming velocity. as3mt mutants developed steatosis, a hallmark of mitochondrial dysfunction. Restoring As3mt in hepatocytes of as3mt mutants rescued steatosis and mitochondrial gene expression. Overexpression of As3mt in wild-type hepatocytes protected against steatosis caused by iAs induced. This demonstrates a novel, conserved, endogenous role for As3mt in hepatic energy metabolism, identifies As3mt loss as a previously unrecognized cause of steatosis, and suggests that arsenic may induce mitochondrial dysfunction due to sequestering As3mt from its endogenous role. - Source: PubMed
Publication date: 2026/05/02
Delaney PatriceGriffin JamesKhan NoufIbrash BalnurO'Connor Matthew JVenit TomasAmbrosio Elizabeth MayelaPergantis Spiros AOber ElkePercipalle PiergiorgioSadler Kirsten C - Alzheimer's disease (AD) is characterized by progressive neurodegeneration driven by tau and amyloid-β (Aβ) pathology, although the underlying molecular mechanisms remain incompletely understood. Emerging evidence implicates altered DNA methylation (DNAm) in AD but comprehensive analyses in experimental models are limited. Here, we profile DNAm dynamics in two widely used transgenic mouse models of tau (rTg4510) and Aβ (J20) neuropathology, focusing on the entorhinal cortex and hippocampus. Using reduced representation bisulfite sequencing (RRBS) and methylation arrays across multiple disease stages, we identified widespread pathology-associated DNAm alterations in both models. Tau pathology in rTg4510 mice was associated with extensive DNAm remodeling at genes involved in neuronal plasticity, apoptosis, and lipid metabolism, including , , and . In contrast, J20 mice exhibited more modest changes, primarily at immune-related loci such as , , and . Tau-associated DNAm changes were more consistent across brain areas than those associated with Aβ pathology. Comparison with human AD DNAm datasets revealed overlapping DNAm differences, including hypermethylation at and in rTg4510 mice. These findings provide robust evidence for early, pathology-associated epigenetic alterations in AD and highlight the utility of epigenomic profiling in transgenic models for identifying novel targets for early intervention in AD. - Source: PubMed
Publication date: 2026/04/07
Leung Szi KayWalker Emma MPolicicchio StefaniaDahir AishaVellame Dorothea SeilerSmith Adam RSwarbrick RhianLunnon KatieDempster Emma LAhmed ZeshanHannon EilisCastanho IsabelMill Jonathan - - Source: PubMed
Publication date: 2026/03/17
Bao Jia-ChengYang YuanWang YiXie Fu-Sheng - Folate is an essential nutrient that supports the formation of S-adenosyl methionine (SAM) in the pathway of one carbon metabolism. Dietary folate intake has been shown to affect the SAM-dependent methylation of diverse substrates, including DNA and inorganic arsenic (iAs). The methylation of iAs by arsenic methyltransferase (AS3MT) plays a key role iAs detoxification in both humans and mice. Our recent studies using wild-type C57BL/6N mice showed that preconception exposure to iAs resulted in heritable changes in DNA methylation in paternal sperm and differential expression of genes in tissues of the offspring that developed a diabetic phenotype. The goal of the present study was to determine if dietary folate can modify the iAs-induced differential methylation of DNA in sperm of male C57BL/6 mice expressing the human AS3MT and exhibiting a human-like pattern of iAs metabolism. Mice were fed folate deficient (FD, 0 mg folic acid/kg) or folate supplemented (FS, 10 mg folic acid/kg) diet for 6 weeks, followed by exposure to 0 (controls) or 400 ppb iAs (arsenite) in drinking water for 5 weeks while on the same types of diet. Reduced Representation Bisulfite Sequencing was used to identify CpG sites and genes that were differentially methylated in response to iAs exposure, followed by analysis of pathways enriched for these genes. Genes and pathways associated with cell morphology and function, and neural structure and function were the top pathways enriched by iAs exposure in both FD and FS mice. Notably, pathways associated with diabetes, regulation of insulin secretion and signaling were enriched for differentially methylated genes only in the sperm of iAs-exposed FS mice. These results suggest that folate intake modifies the effects of iAs exposure on DNA methylation in sperm of the humanized mice, providing strong rationale for studies that will examine the role of folate in modulation of adverse effects of preconception exposure to iAs. - Source: PubMed
Publication date: 2026/03/10
Shang BingzhenDouillet ChristelleHartwell HadleyMiller MadisonCable PeterShi QingZou FeiKrupenko Sergey AIderaabdullah Folami Yde Villena Fernando Pardo-ManuelFry Rebecca CStýblo Miroslav