DDAH1 Antibody
Description
What is DDAH1 Antibody?
DDAH1 antibodies are immunoreagents designed to detect and quantify the DDAH1 enzyme in experimental models. These antibodies are pivotal for understanding DDAH1’s function in regulating nitric oxide (NO) bioavailability by degrading ADMA, a molecule linked to endothelial dysfunction and cardiovascular diseases .
Vascular and Endothelial Studies
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DDAH1 antibodies identified endothelial-specific expression in mice, linking its deletion to elevated ADMA levels, reduced NO production, and hypertension .
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Paradoxically, a 2015 study using endothelium-specific DDAH1-knockout mice found no changes in plasma ADMA or blood pressure, but impaired angiogenesis, highlighting cell-autonomous roles in endothelial function .
Cellular and Molecular Insights
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In human umbilical vein endothelial cells (HUVECs), DDAH1 knockdown via siRNA reduced cyclin D1 expression and arrested the cell cycle at G1/G2 phases, implicating DDAH1 in endothelial proliferation .
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DDAH1 antibodies detected expression in non-endothelial cells (hepatocytes, neurons, renal cells), challenging the notion of endothelial exclusivity .
Genetic and Clinical Correlations
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A DDAH1 promoter polymorphism (−396 4N ins/del) reduced transcriptional activity by 40% in human lymphocytes, correlating with elevated stroke risk .
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Immunohistochemistry using DDAH1 antibodies localized the enzyme to neuronal processes in human brain tissue, suggesting roles beyond cardiovascular biology .
Validation and Specificity
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Knockout Controls: Antibodies like ab180599 demonstrated specificity using DDAH1-knockout A431 cell lysates, showing no off-target bands .
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Tissue Staining: Proteintech’s antibody revealed DDAH1 in vascular endothelium across multiple organs, consistent with its role in systemic ADMA clearance .
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Post-Translational Modifications: Discrepancies between observed (35–37 kDa) and predicted (31 kDa) molecular weights suggest glycosylation or other modifications .
Implications for Therapeutic Development
DDAH1 antibodies are instrumental in studying ADMA-related pathologies, such as hypertension and atherosclerosis. Targeting DDAH1 could modulate NO pathways, offering potential therapies for cardiovascular diseases .
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
- DDAH1 is involved in the MiR-21-mediated DDAH1/ADMA/NO signaling pathway. PMID: 29682517
- DDAH-1 expression is associated with the promotion of the angiogenesis stimulating factor VEGF. PMID: 28741166
- Research suggests that DDAH1 acts as a tumor suppressor in gastric cancer (GC) and may serve as a diagnostic and prognostic biomarker for GC. PMID: 28580735
- Evidence indicates that DDAH1 deficiency promotes epithelial to mesenchymal transition in renal proximal tubular epithelial cells, leading to fibrosis, and oxidative stress in aging and diabetic kidneys. This study provides direct evidence that DDAH1 significantly affects kidney fibrosis and oxidative stress induced by aging or diabetes. PMID: 28594240
- Findings confirm DDAH1 3'-UTR as a target for miR-21, with endogenous miR-21 exhibiting an increased inhibitory effect on the DDAH1-V3 transcript. PMID: 27663503
- Inflammatory factors expressed in response to myocardial ischemia contribute to the up-regulation of DDAH1. PMID: 28145161
- DDAH1 plays dual roles in a particular matter-induced cell death in alveolar epithelial cells. PMID: 26996393
- The rs3087894 variant in DDAH1 is significantly associated with hypertension and exhibits conflicting results in different ethnic groups. This makes it a suitable candidate for further investigations to elucidate the mechanisms of hypertension in various populations. PMID: 26786611
- The wild-type rs480414 variant demonstrates 92% sensitivity and 53% specificity for pulmonary hypertension in bronchopulmonary dysplasia. PMID: 26663142
- Results indicate that miR-21 may regulate renal fibrosis through the Wnt pathway by directly targeting DDAH1. PMID: 26455824
- The most significant associations were detected for PECAM1*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005). PMID: 26662939
- FoxO1 regulates asymmetric dimethylarginine through the downregulation of dimethylaminohydrolase 1 in HUVECs and subjects with carotid atherosclerosis. PMID: 26226438
- Gene-based analyses revealed associations of the DDAH1 gene with longitudinal blood pressure phenotypes, associations with essential hypertension, blood pressure salt sensitivity, preeclampsia, or preclinical stages of atherosclerosis. PMID: 25424718
- DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis. PMID: 24260221
- The advanced glycation end products-receptor for advanced glycation end products-mediated reactive oxygen species generation could be involved in endothelial dysfunction in diabetic end-stage renal disease patients. PMID: 23766377
- DDAH1 genotypes were closely related to asymmetric dimethylarginine levels, but not to measures of endothelium-dependent vasodilation in an elderly population. PMID: 23892448
- Only the DDAH1-V1 transcript is responsible for ADMA metabolism, and transcript-specific primers are recommended to determine DDAH1 mRNA expression. PMID: 23864585
- Elevated asymmetric dimethylaginine is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature coronary artery disease. PMID: 23022711
- A significant decrease in asymmetric dimethylarginine levels was found in ex-extremely low birth weight young adults compared to term birth weight young adults. PMID: 21420186
- Data suggest that estradiol alone has no effect on the DDAH/asymmetric dimethylarginine/nitric oxide pathway in arterial endothelium, but it counters oxidized LDL; estradiol restores DDAH activity and prevents the loss of eNOS (nitric oxide synthase 3). PMID: 22982060
- DDAH1 gene DNA methylation plays a crucial role in the pathogenesis of idiopathic pulmonary fibrosis. PMID: 22700861
- Genetic polymorphisms in DDAH genes influence serum ADMA levels in individuals with T1 diabetes mellitus. PMID: 22521321
- High DDAH1 is associated with pediatric diffuse intrinsic pontine glioma. PMID: 22492959
- Non-diabetic hypertensive subjects with a hypertensive response to exercise compared to those with a normal response were characterized by augmented asymmetric dimethylarginine and osteoprotegerin levels. PMID: 21975354
- No association with pre-eclampsia was found. PMID: 21174581
- In acute congestive heart failure, acute renal impairment function, and the modulation of metabolism and extracellular transport by the DDAH-1/CAT-1 system determine high ADMA and SDMA levels after therapy for acute congestive heart failure. PMID: 21722652
- Data show that DDAH inhibition reduces fibroblast-induced collagen deposition in an ADMA-independent manner and reduces abnormal epithelial proliferation in an ADMA-dependent manner. PMID: 21677199
- HDL significantly increased the attenuated endothelial cell NO production induced by ox-LDL, which was attributed to its effect on the DDAH/ADMA pathway. PMID: 21264497
- Research indicates that DDAH1 is required for metabolizing asymmetrical dimethylarginine and N(omega)-monomethyl-L-arginine. PMID: 21493890
- Results provide evidence that the SNP rs1241321 in DDAH1 is associated with type 2 diabetes and its long-term outcome. PMID: 21303562
- DDAH1 plays a unique role in activating Akt that affects endothelial function independently of degrading endogenous nitric oxide synthase inhibitors. PMID: 21212404
- Recent studies suggest that DDAH may regulate endothelial nitric oxide activity and endothelial function through both asymmetric dimethylarginine-dependent and -independent mechanisms. PMID: 19682581
- Expression of hDDAH1 messenger RNA is found in all organs of DDAH1 transgenic mice investigated, whereas human DDAH1 is absent in wild-type littermates. PMID: 19666120
- Circulating methylarginine levels and the decline in renal function in patients with chronic kidney disease are modulated by DDAH1 polymorphisms. PMID: 20010544
- Results suggest that the DDAH1 loss-of-function polymorphism is associated with both increased risk of thrombosis stroke and coronary artery disease in the Chinese Han population. PMID: 20167924
- Recombinant human DDAH1 overexpression protects transgenic mice from adverse structural and functional changes in cerebral arterioles in hyperhomocysteinemia but not from accelerated carotid artery thrombosis induced by the HM/LF diet. PMID: 20019334
- The enzyme that hydrolyzes methylated inhibitors of nitric oxide synthase is present in circulating human red blood cells. PMID: 11811522
- The first evidence of the importance of DDAH1 polymorphisms in pre-eclampsia susceptibility was provided. PMID: 15501905
- By increasing the synthesis of the proangiogenic factor nitric oxide, DDAH promotes postnatal angiogenesis and arteriogenesis. PMID: 15781754
- DDAH-1 and DDAH-2 messenger RNA and protein were demonstrated in first trimester placental tissue, primary extravillous trophoblasts, and extravillous trophoblast-derived cell lines. PMID: 16920729
- It is concluded that L-arginine regulates asymmetric dimethylarginine (ADMA) metabolism dose-dependently by competing for DDAH, thus maintaining the metabolic balance of L-arginine and ADMA, and endothelial NO homeostasis. PMID: 17075694
- DDAH-1 activity leads to the accumulation of asymmetric dimethylarginine and a reduction in nitric oxide signaling. PMID: 17273169
- Research demonstrates a critical role for DDAH-1 and endogenous methylarginines in the pathogenesis of endothelial dysfunction. PMID: 17881609
- Human dimethylarginine dimethylaminohydrolase-1 is inhibited by S-nitroso-L-homocysteine and hydrogen peroxide. PMID: 17895252
- The maintenance of normoglycemia, not glycemia-independent actions of insulin, maintained dimethylarginine tissue levels by preserving physiological DDAH activity. PMID: 18292189
Customer Reviews
Applications : WB
Sample type: Human HT-29 cell
Sample dilution: 1:1000
Review: Compounds #1–5 downregulated DDAH1 and DDAH2 protein expression at 200 µM, by 2.2, 22.8, 72.8, 4.4, and 299-fold (DDAH1) and by 10.8, 29.5, 8.9, 2.6, and 24.3-fold (DDAH2), respectively.
