N-methylation is one method by which drug and other xenobiotic compounds are metabolized by the liver. NNMT responsible for this enzymatic activity which uses S-adenosyl methionine as the methyl donor
- Known as:
- N-methylation measurement drug xenobiotic compounds metabolized liver. NNMT responsible enzymatic activity uses S-adenosyl methionine methyl donor
- Catalog number:
- 29-728
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- N-methylation one method which drug and other xenobiotic compounds are metabolized the liver. NNMT responsible for this enzymatic activity uses S-adenosyl methionine methyl donor
Related genes to: N-methylation is one method by which drug and other xenobiotic compounds are metabolized by the liver. NNMT responsible for this enzymatic activity which uses S-adenosyl methionine as the methyl donor
- Gene:
- NNMT NIH gene
- Name:
- nicotinamide N-methyltransferase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-18
- Date modifiied:
- 2014-11-19
Related products to: N-methylation is one method by which drug and other xenobiotic compounds are metabolized by the liver. NNMT responsible for this enzymatic activity which uses S-adenosyl methionine as the methyl donor
5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: 5-[6-Methoxy-2-methoxytritylamino-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol C4413C2H45N4NO5 CAS:
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Specifically designed for converting microscope slides and films/film slides into digital data formats with high resolution"'Enduroä PAGE 2D System, includes 2D insert and PAGE System components'Enduroä PAGE Electroblotting System, includes the blotting insert and PAGE system components'VX-200 Vortex Mixer Optional head attachment for 24 x 1.5/2.0 ml tubes, 24 x 0.5 ml tubes and 32 x 0.2 ml tubes (or 4 tube strips)'VX-200 Vortex Mixer Optional head attachment for 8 x 15 ml and 8 x 12/13 mm diameter tubes(+)-(1-Oxyl-2,2,5,5-tetramethylpyrrolidin-3-yl)methyl Methanethiosulfonate C10H20NO3S2 CAS: 681034-14-0(+)-(1-Oxyl-2,2,5,5-tetramethylpyrrolidin-3-yl)methyl Methanethiosulfonate CAS: 681034-14-0 Formula: C10H20NO3S2(+)-(2S,6Z,9S,10E)-9-{[tert-Butyl(dimethyl)silyl]oxy}-2,6,10-trimethyl-11-(2-methyl-1,3-thiazol-4-yl)-undeca-6,10-dien-1-ol C24H43NO2SSi CAS: 210690-99-6(+)-(2S,6Z,9S,10E)-9-{[tert-Butyl(dimethyl)silyl]oxy}-2,6,10-trimethyl-11-(2-methyl-1,3-thiazol-4-yl)-undeca-6,10-dien-1-ol CAS: 210690-99-6 Formula: Related articles to: N-methylation is one method by which drug and other xenobiotic compounds are metabolized by the liver. NNMT responsible for this enzymatic activity which uses S-adenosyl methionine as the methyl donor
- Heterogeneous circulating tumor cell (CTC) clusters interact with platelets, neutrophils, stromal cells, and immune cells, forming a protective state that may facilitate survival in the circulation and metastatic dissemination. Nicotinamide N-methyltransferase (NNMT) is associated with metabolic reprogramming, stromal activation, epithelial-mesenchymal plasticity, and immune suppression. However, its coordinated relationship with platelet/coagulation, neutrophil/ neutrophil extracellular trap (NET), and immune exhaustion programs in CTC-associated states has not been systematically evaluated. Therefore, we constructed a hypothesis-generating framework integrating mechanistic evidence, pan-cancer computational analyses, and single-cell transcriptomic analyses. - Source: PubMed
Publication date: 2026/09/10
Gong JiayangWang ZheShi YunRen MinlanLi TingtingLi GangPeng Rui - Systemic sclerosis (SSc) is characterized by fibroblast activation and fibrosis of the skin and multiple organs. Metabolic reprogramming is a critical determinant of fibroblast fate. Nicotinamide N-methyltransferase (NNMT), which links NAD metabolism with cellular methylation pathways, has emerged as a regulator of fibroblast activation. To investigate how NNMT modulates profibrotic fibroblast programming and skin fibrosis, the effects of the bisubstrate-like NNMT inhibitor II559 were examined in transforming growth factor-β (TGF-β)-stimulated foreskin, healthy, and SSc skin fibroblasts, and in bleomycin-induced skin fibrosis in mice. Fibrotic gene expression, extracellular matrix (ECM) production, metabolic intermediates, and H3K27-associated chromatin methylation was assessed. Treatment with II559 suppressed TGF-β-induced myofibroblast differentiation and reduced stimulation of profibrotic genes in healthy fibroblasts, and attenuated constitutive fibrotic gene expression and ECM secretion in SSc fibroblasts. Mechanistically, NNMT inhibition lowered 1-methylnicotinamide levels (1-MNA), restored methylation potential, and increased repressive H3K27me3 chromatin marks. In bleomycin-treated mice, NNMT inhibition reduced dermal thickening and collagen accumulation while preserving dermal white adipose tissue. These changes were accompanied by restoration of NAD homeostasis and methylation balance. These findings identify NNMT as a cell-autonomous regulator of metabolic and epigenetic reprogramming in fibroblasts and support pharmacologic NNMT inhibition as a potential therapeutic strategy for SSc skin fibrosis. - Source: PubMed
Publication date: 2026/09/09
Saba KamalKataria SunnyShi BoKumar UmeshVerma PriyankaKeyorkgy JohnWalters GabrielChini Claudia C SChini Eduardo NZhao TianqiIyamu Iredia DHuang RongTsou Pei-SuenAmin M AsifVarga John - Embryo implantation critically depends on the establishment of endometrial receptivity, which is governed by progesterone-driven stromal decidualization during the mid-secretory phase. In recurrent implantation failure (RIF), this process is frequently disrupted, yet the molecular mechanisms remain unclear. Here, through integrative analysis of bulk and single-cell transcriptomic datasets, we identified nicotinamide N-methyltransferase (NNMT) as one of the most significantly downregulated genes in the endometrium of RIF patients. Temporal profiling of human endometrial samples across the menstrual cycle revealed progressive upregulation of NNMT from proliferative to secretory phase, while in hormonally induced stromal cell differentiation, NNMT expression rose sharply from day 4 onward. Functional assays demonstrated that NNMT knockdown impaired decidualization, as evidenced by reduced expression of PRL and IGFBP1 and attenuated cytoskeletal reorganization. Mechanistically, NNMT deficiency increased intracellular S-adenosylmethionine levels, enhanced the expression of core PRC2 components, and promoted H3K27me3 enrichment at the promoters of decidual genes, consistent with their transcriptional repression. Pharmacologic inhibition of histone methylation by 3-deazaneplanocin A or selective EZH2 inhibition by GSK126 partially rescued both molecular and morphological defects in NNMT-deficient stromal cells. In vivo, uterine NNMT silencing in pregnant mice also increased H3K27me3 level, reduced the expression of decidualization-related genes, and decreased the number of implantation sites. Collectively, our findings identify NNMT as a metabolic-epigenetic regulator of endometrial receptivity, and support its potential as a candidate biomarker for RIF. - Source: PubMed
Publication date: 2026/09/07
Yang BinPeng LinZhao ChenxiZeng YuqiDeng YanqingTian LifengZhao YanFan HanchengLin JiayingHuang Jialyu - Cardiometabolic heart failure with preserved ejection fraction (HFpEF) is characterized by the frequent co-occurrence of obesity, central adiposity, insulin resistance, type 2 diabetes mellitus, and low-grade inflammation. How these exposures sustain myocardial remodeling remains uncertain. One-carbon metabolism provides a plausible biochemical interface between nutrient stress and epigenetic regulation: S-adenosylmethionine (SAM) donates methyl groups, whereas S-adenosylhomocysteine (SAH) inhibits methyltransferases. Altered nicotinamide N-methyltransferase (NNMT) flux, homocysteine-related SAH retention, and metabolic regulation of DNA methyltransferase (DNMT) and ten-eleven translocation (TET) enzymes could therefore reshape DNA methylation and hydroxymethylation. Direct human evidence remains sparse: available HFpEF methylation data are blood-derived rather than myocardial, and cardiac or adjacent models support individual components of the framework but not a continuous disease-specific pathway. We therefore view DNA methylation as a context-dependent regulatory layer that may amplify or stabilize inflammatory, fibrotic, and metabolic programs rather than as a uniform initiating cause. Accordingly, translational studies should prioritize compartment-specific target engagement, reversibility, and biomarker-guided patient selection rather than assume a role for methylation-directed therapy. - Source: PubMed
Publication date: 2026/08/20
Luo WeichenZuo WenjieXu YangYang MingmingJi ZhenjunMa Genshan - Biallelic pathogenic variants in SORD (Sorbitoldehydrongenase gene), encoding sorbitol dehydrogenase, are a common cause of autosomal recessive axonal Charcot-Marie-Tooth disease type 2 (CMT2). Recent evidence suggests direct involvement of skeletal muscle in addition to peripheral nerve degeneration. We investigated muscle biopsies from 4 genetically confirmed CMT-SORD patients using an integrative approach. Histological evaluation revealed features of chronic denervation with grouped fiber atrophy, fiber-type grouping and central nuclei, ie, non-specific neurogenic muscle atrophy. Ultrastructural studies demonstrated mitochondrial abnormalities and expansion of the sarcoplasmic reticulum (SR). Proteomic profiling identified 220 significantly dysregulated proteins in CMT-SORD muscle, including alterations in mitochondrial complex I components, redox enzymes, and metabolic regulators distinct from changes observed in other rare recessive CMTs. Quantitative PCR validated increased levels of NNMT, POSTN, TACO1, as well as complement and immunomodulatory factors, suggesting mitochondrial stress, compensatory metabolic activation and tissue remodeling. Despite mitochondrial vulnerability, serum studies indicated that GDF-15 and FGF-21 did not appear to be suitable biomarkers for CMT-SORD. These findings demonstrate that SORD deficiency induces molecular and structural changes in skeletal muscle that extend beyond denervation, implicating impaired sorbitol metabolism, oxidative stress, and mitochondrial dysfunction as intrinsic myopathic features of SORD-related CMT2. They indicate the need for therapeutic strategies targeting both neuronal and muscular compartments. - Source: PubMed
Publication date: 2026/08/19
Kölbel HeikeHentschel AndreasPreuße CorinnaTiet MayDohrn Maike FMuhmann Davidvan den Ameele JelleChen LeiSchara-Schmidt UlrikeWeis JoachimHorvath RitaMensch AlexanderRoos Andreas