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NOS2 — PRKAA2

Text-mined interactions from Literome

Fleming et al., Thromb Haemost 2003 : AMP activated protein kinase (AMPK) regulates the insulin induced activation of the nitric oxide synthase in human platelets
Giri et al., J Neurosci 2004 (Inflammation) : A pharmacological activator of AMPK , 5-amino-4-imidazole carboxamide riboside ( AICAR ) inhibited lipopolysaccharide (LPS) induced expression of proinflammatory cytokines ( tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 ) and inducible nitric oxide synthase in primary rat astrocytes, microglia, and peritoneal macrophages
Pilon et al., J Biol Chem 2004 : Here we show that pharmacological activation of AMPK by insulin sensitizing drugs markedly inhibits inducible nitric-oxide synthase (iNOS) , a proinflammatory mediator in endotoxic shock and in chronic inflammatory states including obesity linked diabetes ... AMPK mediated iNOS inhibition was observed in several cell types ( myocytes, adipocytes, macrophages ) and primarily resulted from post-transcriptional regulation of the iNOS protein
Di Marco et al., Mol Cell Biol 2005 (Wasting Syndrome) : Moreover, we show that HuR regulates iNOS expression in an AMP activated protein kinase (AMPK) dependent manner
Ropelle et al., Endocrinology 2007 (Anorexia...) : In parallel, the pharmacological activation of hypothalamic AMPK in TB animals markedly reduced the hypothalamic production of inducible nitric oxide synthase , IL-1beta, and TNF-alpha and modulated the expression of proopiomelanocortin, a hypothalamic neuropeptide that is involved in the control of energy homeostasis
Vázquez-Chantada et al., Hepatology 2009 : Because AMPK is activated by the tumor suppressor kinase LKB1, and AMPK activates endothelial nitric oxide ( NO ) synthase ( eNOS ), and NO synthesis is of great importance for hepatocyte proliferation, we hypothesized that in hepatocytes HGF may induce the phosphorylation of LKB1, AMPK, and eNOS through a process regulated by SAMe, and that this cascade might be crucial for hepatocyte growth
Łabuzek et al., Neurotoxicology 2010 : Furthermore, we found that the effects of AICAR on IL-6 and TNF-alpha ( 12, 24h ) release and on the expression of iNOS and NF-kappaB p65 are not AMPK dependent because the pre-treatment of LPS activated microglia with compound C ( a pharmacological inhibitor of AMPK ) did not reverse the effect of AICAR
Shin et al., BMB Rep 2010 : Transduced PEP-1-AMPK inhibits the LPS induced expression of COX-2 and iNOS in Raw264.7 cells
Bradley et al., Arterioscler Thromb Vasc Biol 2010 : Activation of AMPK by AICAR activates endothelial nitric oxide synthase in arteriolar endothelium by increasing its Ser1177 phosphorylation, which leads to vasodilation of resistance arteries and recruitment of microvascular perfusion in muscle
Łabuzek et al., Pharmacol Rep 2010 : Furthermore, the effects of metformin on the release of IL-1ß, IL-6, IL-10, TGF-ß, NO, and ROS as well as on the expression of arginase I, iNOS , NF-?B p65 and PGC-1a were not AMPK dependent , because pretreatment of LPS activated microglia with compound C, a pharmacological inhibitor of AMPK, did not reverse the effect of metformin
Lee et al., Mol Cells 2010 : Furthermore, mitochondrial dysfunction increased the expression of the inducible nitric oxide synthase (iNOS) gene and the production of nitric oxide ( NO ), but NO production was prevented by compound C and mutant dominant negative AMPK ( AMPK-K45R )
Centeno-Baez et al., Am J Physiol Endocrinol Metab 2011 : Resveratrol inhibition of inducible nitric oxide synthase in skeletal muscle involves AMPK but not SIRT1 ... We have previously reported that AMPK activators inhibit inducible nitric oxide synthase (iNOS) , a key proinflammatory mediator of insulin resistance in endotoxemia and obesity