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Dimethylarginine dimethylaminohydrolase 2 (DDAH2) is a protein encoded by the DDAH2 gene and classified as a putative hydrolase. While it shares sequence similarity with DDAH1, which hydrolyzes asymmetric dimethylarginine (ADMA), DDAH2 does not hydrolyze ADMA or participate directly in ADMA metabolism[1]. Instead, DDAH2 contributes to vascular and metabolic homeostasis by inducing the expression of vascular endothelial growth factor (VEGF) via phosphorylation of SP1, a process independent of nitric oxide and NO synthase activity[1][4]. DDAH2 expression is regulated by acetylation and transcription factors such as NF-κB, with relevance for renal nitric oxide signaling[2]. Genetic and transcriptional modulation of DDAH2 has been associated with conditions such as chronic kidney disease, cardiovascular dysfunction, sepsis, and pre-eclampsia[3][4]. It does not currently have direct interacting drugs or a defined mechanism of drug action, and its role as a biomarker is limited compared to DDAH1[3][4].
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