Literature summary for 3.5.3.1 extracted from

Jung, A.S.; Kubo, H.; Wilson, R.; Houser, S.R.; Margulies, K.B.
Modulation of contractility by myocyte-derived arginase in normal and hypertrophied feline myocardium (2006), Am. J. Physiol. Heart Circ. Physiol., 290, H1756-H1762.

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Inhibitors

Inhibitors	Comment	Organism	Structure
S-(2-boronoethyl)-L-cysteine	inhibition results in in reduced fractional shortening, maximal rate of shortening, and relengthening of myocyte contractions	Felis catus

Organism

Organism	UniProt	Comment	Textmining
Felis catus	-	isoforms arginase-I and arginase-II	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
heart	normal and hypertrophied feline myocardium, both isoforms arginase-I and arginase-II in crude myocardial homogenate. Arginase-I is downregulated in left ventricular hypertrophy	Felis catus	-
myocyte	isolated cardiac myocyte shows only isoform arginase-I	Felis catus	-

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Release 2023.1 (January 2023)