Literature summary for 2.1.4.1 extracted from

Faller, K.M.E.; Atzler, D.; McAndrew, D.J.; Zervou, S.; Whittington, H.J.; Simon, J.N.; Aksentijevic, D.; Ten Hove, M.; Choe, C.U.; Isbrandt, D.; Casadei, B.; Schneider, J.E.; Neubauer, S.; Lygate, C.A.
Impaired cardiac contractile function in arginine glycine amidinotransferase knockout mice devoid of creatine is rescued by homoarginine but not creatine (2018), Cardiovasc. Res., 114, 417-430 .

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Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
L-arginine + glycine	Mus musculus	-	L-ornithine + guanidinoacetate	-	?

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
L-arginine + glycine	-	Mus musculus	L-ornithine + guanidinoacetate	-	?

Synonyms

Synonyms	Comment	Organism
AGAT	-	Mus musculus
arginine:glycine amidinotransferase	-	Mus musculus

General Information

General Information	Comment	Organism
malfunction	enzyme-deficient mice develop cardiac dysfunction. Enzyme-deficient mice have rescuable changes in body water and organ weights suggesting a role for creatine as a compatible osmolyte. Creatine-naive enzyme-deficient mice have haemodynamic impairment with low left ventricular systolic pressure and reduced inotropy, lusitropy, and contractile reserve	Mus musculus

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Release 2023.1 (January 2023)