Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) is an essential enzyme capable of degrading asymmetric dimethylarginine, which is an endogenous inhibitor of nitric oxide synthase. Increased expression of DDAH1 and subsequent increased NO production are associated with carcinogenesis. In particular, DDAH1 is involved in the creation of a vascular network by tumor cells, vasculogenic mimicry, which is closely associated with tumor progression and poor patient prognosis. This is the reason why DDAH1 may be a potential therapeutic target for the treatment of cancer.
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[DDAH1 protein: biological functions, role in carcinogenesis processes].
Arkh Patol
February 2025
N.N. Petrov National Medical Research Center of Oncology, St. Petersburg, Russia.
Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) is an essential enzyme capable of degrading asymmetric dimethylarginine, which is an endogenous inhibitor of nitric oxide synthase. Increased expression of DDAH1 and subsequent increased NO production are associated with carcinogenesis. In particular, DDAH1 is involved in the creation of a vascular network by tumor cells, vasculogenic mimicry, which is closely associated with tumor progression and poor patient prognosis.
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February 2025
Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smetna Street, 31-343, Krakow, Poland. Electronic address:
l-arginine derivatives (ADMA, SDMA, NMMA) are endogenous inhibitors of nitric oxide (NO֗) production, which is essential in critical brain processes including blood-brain barrier (BBB) integrity and long-term potentiation (LTP). ADMA and NMMA are degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and protein arginine methyltransferase 5 (PRMT5) is an emerging epigenetic enzyme that mainly represses transcription of target genes via symmetric dimethylation of arginine residues. There is no data concerning the impact of metabotropic glutamate receptors (mGlu) ligands on this aspect of brain physiology.
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Shenyang Medical College, No.146, Huanghe North Street, Yuhong District, Shenyang, Liaoning Province 110034, China. Electronic address:
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Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is a critical enzyme that regulates nitric oxide (NO) signaling through the degradation of asymmetric dimethylarginine (ADMA). Previous studies have revealed a link between the beneficial effects of aerobic exercise and the upregulation of DDAH1 in bones and hearts. We previously reported that skeletal muscle DDAH1 plays a protective role in cardiotoxin (CTX)-induced skeletal muscle injury and regeneration.
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Department of Pharmaceutical Sciences, University of Perugia, via del Liceo 1, 06123 Perugia, Italy.
Dimethylarginine dimethylaminohydrolase-1 (DDAH-1) accounts for the catabolism of the endogenous inhibitors of nitric oxide (NO) synthases, namely, ADMA (,-dimethyl-l-arginine) and NMMA (-monomethyl-l-arginine). Inhibition of DDAH-1 may prove a therapeutic benefit in diseases associated with elevated nitric oxide (NO) levels by providing a tissue-specific increase of ADMA and NMMA. In this work, we have used molecular dynamics to generate a pool of DDAH-1 conformations in the apo and holo forms.
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