Gene interactions and pathways from curated databases and text-mining

◀ Back to NOX1

MMP9 — NOX1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Abe et al., Life Sci 2006 : Diphenylene iodonium, an inhibitor of NADPH oxidase , had a similar effect on MMP-9 activity
Spallarossa et al., Cardiovasc Res 2006 (MAP Kinase Signaling System) : Inhibition of NAD ( P ) H oxidase attenuates the increase in MMP-2, but augments the doxorubicin induced increase in MMP-9
Cook-Mills et al., Cell Mol Biol Incl Cyto Enzymol 2006 : The endothelial cell NADPH oxidase and endothelial cell MMP activities are required for VCAM-1 dependent lymphocyte migration as determined by scavenging of ROS, by pharmacologic or antisense inhibition of NADPH oxidase and by pharmacologic inhibition of endothelial cell MMPs
San José et al., Free Radic Biol Med 2009 : Insulin mediated NADPH oxidase activation stimulated MMP-9 activation in monocytes and cell proliferation in macrophages
Jagadeesha et al., Cardiovasc Res 2012 (MAP Kinase Signaling System) : The Nox1 NADPH oxidase signals through EGFR to activate MMP-9 and promote the shedding of N-cadherin, thereby contributing to SMC migration
Xu et al., J Vasc Res 2012 (Neointima) : Following vascular injury, the increased expression of Nox1 in SMCs within the neointima initiates redox dependent phosphorylation of ERK1/2 and subsequent MMP-9 activation
Hsieh et al., Journal of neuroinflammation 2012 : These results demonstrated that in RBA-1 cells, activation of ATF2/AP-1 by the PKC ( a ) -mediated Nox ( 2 ) /ROS signals is essential for upregulation of MMP-9 and cell migration enhanced by LTA
Lin et al., Cell communication and signaling : CCS 2012 : These results demonstrated that in RBA-1 cells, activation of AP-1 ( c-Fos/c-Jun ) by the PKC-a mediated Nox2/ROS signals is essential for up-regulation of MMP-9 and cell migration enhanced by BK
Kuo et al., Int J Immunopathol Pharmacol 2013 (Anoxia...) : KMUP-1 protects liver from I/R-injury and hypoxic hepatocytes from apoptosis associated free radical generation and pro-inflammation by restoring/increasing NO/cGMP/PPAR-gamma, reducing ROS/Nox2 and inhibiting ROCKII/MMP-9