Gene interactions and pathways from curated databases and text-mining

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ARG2 — NOS3

Text-mined interactions from Literome

Baggio et al., J Pharmacol Exp Ther 1999 : We conclude that arginase plays a significant role in the regulation of nitric oxide synthase mediated NANC relaxation in the IAS
Liu et al., Sheng Li Xue Bao 2002 (Cardiomegaly) : L-Arg also increased the gene expression of eNOS
White et al., Hypertension 2006 : Moreover, arginase inhibition restores endothelial NOS signaling and l-arginine responsiveness in old rat aorta
Sasaki et al., Am J Physiol Lung Cell Mol Physiol 2007 (Hypertension, Pulmonary...) : Roles of accumulated endogenous nitric oxide synthase inhibitors, enhanced arginase activity, and attenuated nitric oxide synthase activity in endothelial cells for pulmonary hypertension in rats
Liu et al., Amino Acids 2012 (Birth Weight) : In conclusion, this study demonstrated that dietary Arg or NCG supplementation may affect microRNAs ( miR-15b, miR-222 ) targeting VEGFA and eNOS gene expressions in umbilical vein, so as to regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue for fetal development and survival, and enhance the reproductive performance of sows
Shin et al., The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2011 : In HUVECs, inhibition of arginase activity by CLE reciprocally increased NOx production through enhancement of eNOS dimer stability without any significant changes in the protein levels of eNOS and arginase II expression
Prieto et al., Placenta 2011 (Anoxia) : We studied in human umbilical vein endothelial cells ( HUVEC ) whether hypoxia reduced NO synthesis results from increased arginase mediated l-arginine metabolism and changes in subcellular localization of eNOS and arginase-2
Krause et al., Placenta 2013 (Fetal Growth Retardation) : We studied whether arginase-2 participates in IUGR related placental vascular dysfunction counteracting eNOS dependent relaxation, and the regulation of arginase-2 and eNOS expression in endothelial cells from IUGR umbilical arteries ( HUAEC ) and veins ( HUVEC )