Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
- Known as:
- Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
- Catalog number:
- enz-014
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
Related genes to: Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
- 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: Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
Related articles to: Recombinant Human Dimethylarginine Dimethylaminohydrolase 1 DDAH1
- 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 - MicroRNA (miRNA) has been confirmed to be related to gene expression regulation and disease progression. However, the role of miR-155-5p in diabetic retinopathy remains unclear. - Source: PubMed
Publication date: 2026/02/02
Dou WenwenFu ChangboJin LeiLi TingLi Mingxing - Air pollution has been implicated in various adverse health effects, including neurodevelopmental and neurodegenerative impairments. However, the long-term impact of early-life ultrafine particle (UFP) exposure on the brain remains poorly understood. Using a sequential exposure mouse model, we investigated how early-life ultrafine carbonaceous particles (UFP) exposure programs neurobehavioural and molecular vulnerability upon adult re-exposure. Wild-type C57BL/6J mice were exposed to either HEPA-filtered air or UFP during the prenatal (gestational days 8-9 and 16-17) and/or postnatal periods (postnatal days 4-7 and 10-13), followed by a 4-day re-exposure in adulthood (postnatal days 142-145). Behavioural assessments revealed hippocampus-dependent spatial memory deficits and anxiolytic-like behaviour following cumulative exposure. Brain proteomic analysis identified reduced protein levels of key modulators of synaptic signalling and neurovascular homeostasis (Erbb4 and Ddah1), accompanied by gene-specific promoter methylation changes and shortened telomere length, indicating persistent epigenetic reprogramming and accelerated cellular aging. We validated the epigenetic sensitivity of ERBB4 to prenatal air pollution in human cord blood from the ENVIRONAGE birth cohort. The integrative design, encompassing behavioural phenotyping and molecular profiling, offers a comprehensive systems-level perspective on the neurobiological effects of UFP. Our findings suggest that developmental UFP exposure induces increased susceptibility to re-exposure on behavioural, epigenetic, and proteomic outcomes. This work provides evidence for UFP as a potentially critical environmental determinant of brain health throughout life. - Source: PubMed
Publication date: 2026/01/09
Vanbrabant KennethRasking LeenAlfano RosellaAmeloot MarcelCraps LarsMartens Dries SVanmierlo TimVangeneugden MaartjeNawrot Tim SSchins Roel P FCassee Flemming RPlusquin Michelle - Lung aging is a multifactorial series of molecular alterations that leads to gradual deterioration of lung function and increased vulnerability to cancer. Tumor communicates with host organs partially through extracellular vesicles; however, the mechanistic drivers and consequences of lung aging in the context of cancer remain unclear. Here we identify cancer cell-secreted dimethylarginine dimethylaminohydrolase-1 (DDAH1) protein induces citrulline accumulation and promotes lung fibrosis and aging. Mechanistically, our single-cell sequencing and genetic knockout mice evidence that citrulline availability elevation inhibits peptidyl arginine deiminase 4-mediated transforming growth factor-β1 (TGF-β1) citrullination, thereby inducing the TGF-β1/Smad3 signaling pathway in lung fibroblasts. Notably, vacuolar protein sorting assists the packaging of DDAH1 into the late endosomes. The administration of DDAH1 inhibitor reduces fibrosis and alleviates lung aging. Conclusively, our findings reveal tumor-derived DDAH1 protein contributes to citrulline accumulation to promote lung aging, shedding light on the treatment and diagnosis of tumors by inhibiting senescent lung fibroblasts. - Source: PubMed
Publication date: 2025/12/24
Liu LiuWang QianyueChen MengZhou HaifengLi XuYuan ZiqiHu YongWang ChaoqunZhang XiaohuiHu ShengWu XiaotingLi MeixinLi JuanjuanChen AijunYan Wei