Literature summary for 3.5.3.18 extracted from

Sydow, K.; Schmitz, C.; von Leitner, E.C.; von Leitner, R.; Klinke, A.; Atzler, D.; Krebs, C.; Wieboldt, H.; Ehmke, H.; Schwedhelm, E.; Meinertz, T.; Blankenberg, S.; Boeger, R.H.; Magnus, T.; Baldus, S.; Wenzel, U.
Dimethylarginine dimethylaminohydrolase1 is an organ-specific mediator of end organ damage in a murine model of hypertension (2012), PLoS ONE, 7, e48150.

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Cloned(Commentary)

Cloned (Comment)	Organism
expressed in Mus musculus	Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
Nomega,Nomega'-dimethyl-L-arginine + H2O	Homo sapiens	-	dimethylamine + L-citrulline	-	?

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	O94760	-	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
Nomega,Nomega'-dimethyl-L-arginine + H2O	-	Homo sapiens	dimethylamine + L-citrulline	-	?

Synonyms

Synonyms	Comment	Organism
DDAH1	-	Homo sapiens
dimethylarginine dimethylaminohydrolase1	-	Homo sapiens

General Information

General Information	Comment	Organism
physiological function	human DDAH1 overexpression does not protect against hypertension-induced cardiac fibrosis and hypertrophy. In addition, the hypertension-induced impairment of the endothelium-dependent vasorelaxation of aortic segments ex vivo is not significantly attenuated by DDAH1 overexpression. However, human DDAH1 overexpressing mice display an attenuated hypertensive inflammatory response in renal tissue, resulting in less hypertensive renal injury	Homo sapiens

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Release 2023.1 (January 2023)