Ask about this productRelated genes to: DDAH1 antibody
- Gene:
- DDAH1 NIH gene
- Name:
- dimethylarginine dimethylaminohydrolase 1
- Previous symbol:
- -
- Synonyms:
- DDAH
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-22
- Date modifiied:
- 2016-10-05
Related products to: DDAH1 antibody
Related articles to: DDAH1 antibody
- Sarcopenia and chronic pain are prevalent age-related conditions with substantial health impacts, yet their causal relationship remains unclear. Our aim is to study the bidirectional causal relationship among these diseases and identify potential therapeutic targets through genetic methods, as well as explore new therapeutic drugs. We performed bidirectional Mendelian randomization and Bayesian colocalization analyses using GWAS data from sarcopenia and chronic pain studies to explore their genetic relationships. Through integrating PheWAS and DrugBank analyses, we identified potential therapeutic candidates. We then evaluated these candidates using FAERS database for safety profiles and explored their pathway-level associations through drug-omics data. Our analyses revealed significant bidirectional genetic associations between sarcopenia and chronic pain, identifying 9 shared genes (MAPKAPK3, MYBPC3, POLR2L, DDAH1, FAM177B, ABCC8, RMDN3, RFTN2, and SUOX). Four genes (MAPKAPK3, DDAH1, ABCC8, and SUOX) were identified as druggable targets, with 18 compounds (including approved, investigational, and preclinical drugs) identified as potential therapeutic candidates. After FAERS screened and excluded candidate drugs that might aggravate muscle or pain symptoms, dexlansoprazole and glipizide showed relatively favorable safety profiles among compounds targeting these genes. Subsequent drug-omics analysis identified pathway enrichments consistent with muscle and pain-related processes, though clinical efficacy remains unestablished. This study provides genetic evidence for a causal bidirectional relationship between sarcopenia and chronic pain, identifying potential therapeutic targets. However, findings are based on computational analyses of summary-level data without experimental validation. The identified drug candidates warrant further rigorous experimental and clinical investigation for repurposing strategies in managing these conditions. - Source: PubMed
Li JuanHuang JiaqiHan Jiang - Pena, Eduardo, Samia El Alam, Juliane Hannemann, and Rainer Böger. Compliance and genetic variability are determinants of the success of l-arginine/l-citrulline supplementation in high altitude-A pilot study. 00:00-00, 2026. - Source: PubMed
Publication date: 2026/05/12
Pena EduardoEl Alam SamiaHannemann JulianeBöger Rainer - Under nutrient deprivation conditions, the liver maintains systemic energy homeostasis by mobilizing lipid reserves, a process often accompanied by hepatic lipid accumulation. Dimethylarginine dimethylaminohydrolase 1 (DDAH1), a key metabolizing enzyme for asymmetric dimethylarginine (ADMA), has been demonstrated to exert a protective effect in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), yet its role in fasting-induced hepatic metabolic adaptation remains incompletely elucidated. In this article, we explored the function of DDAH1 in fasting-induced liver lipid accumulation using hepatocyte-specific knockout ( ) mice. Compared with control mice ( ), mice exhibited significantly attenuated hepatic steatosis after fasting. Lipidomic analysis of the liver revealed decreased levels of most lipid species (e.g., triglycerides and free fatty acids) in mice. Further mechanistic studies demonstrated that deletion downregulated the protein level of hepatic fatty acid binding protein 1 (FABP1) and activated the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway, thereby enhancing autophagic flux and promoting lipid droplet degradation under fasting conditions. Hepatic overexpression of FABP1 reversed the anti-steatotic phenotype of mice, while treatment with the AMPK inhibitor Compound C suppressed autophagy and increased hepatic lipid accumulation. In addition, overexpression of DDAH1 in hepatocytes exacerbated hepatic steatosis in fasted mice, coinciding with FABP1 upregulation and autophagy inhibition. Collectively, this article reveals that DDAH1 plays a critical role in hepatic lipid metabolism under fasting conditions by modulating FABP1 expression and AMPK/mTOR-mediated autophagy. - Source: PubMed
Publication date: 2025/12/04
Luo KaiShen XiyueWang SiyuLi FangJianggewaer YierxiatiSun WeipingLu Zhongbing - Erectile dysfunction (ED) is a multifactorial condition influenced by vascular, neuroendocrine, metabolic, and psychological factors. Growing evidence suggests that genetic variation may contribute to individual susceptibility, severity, and therapeutic response, particularly regarding nitric oxide (NO) signaling and vascular pathways. To systematically synthesize evidence on genetic biomarkers associated with the risk, severity, or therapeutic response of ED in adult men. - Source: PubMed
Publication date: 2026/03/24
Ferezin Letícia PerticarraraKayzuka CezarPaiva de Alcântara E Silva MaurielyTavares Peixeiro Cecilia NogueiraRondon-Pereira Vitória CarolinaTanus-Santos Jose EduardoLacchini Riccardo - Background Gastric cancer (GC) is one of the most common cancers globally. Programmed death cells, a cell-surface molecule, drive arginine dimethylation, disrupting nitric oxide (NO) production in peripheral tissues. Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) axis disruption depends on dimethylarginine dimethylaminohydrolase 1 (DDAH1) activity during metastasis in patients with severe gastritis, either synergizing with NO or inhibiting PD-1/PD-L1 activation in tumor growth. This study aimed to determine the arginine dimethylation process in conjunction with nitrosative stress, which dysregulates the PD-L1 axis in GC cells. Methodology A cross-sectional study was conducted utilizing real-time polymerase chain reaction for relative mRNA expressions, high-performance liquid chromatography for asymmetric dimethylarginine (ADMA)/symmetric dimethylarginine (SDMA) assays, and spectrophotometry for NO analysis. Statistical tools such as RStudio (version 2024.12.1) were used to conduct principal component analysis, heatmaps, and t-tests/analysis of variance or Mann-Whitney/Kruskal-Wallis tests after Shapiro-Wilk post-hoc tests in different groups (GC, disease control, and healthy control). Results We observed abnormal NO production and reduced mitochondrial DNA copy numbers in GC patients. Significantly decreased levels of ADMA and excessive influx of arginase activity were determined in GC patients. PD-L1 expression was significantly higher in GC patients, while suboptimal PD-L1 expression was associated with disease control. The abnormal influx of dimethylated arginine and matrix metalloproteinase-7 (MMP-7) was associated with and linked to NO production levels. Their association could be with the nitrigenic pathway and with possible mechanisms for damaging cell-surface molecules in GC. Conclusions Overall, the disrupted ADMA-SDMA balance and Ca++ permeability impair the regulation of claudin-4, MMP-7, and PD1/PD-L1 in GC patients. These variables hold promise as diagnostic and therapeutic targets for improved GC management. - Source: PubMed
Publication date: 2026/02/12
Priyatma Prakash ShyamMakharia Govind KGupta Siddhartha DSahni PeushSahoo Ranjit KThulkar SanjaySubramanian ArulselviPandey R M