Gene interactions and pathways from curated databases and text-mining

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NOX3 — VCAM1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Matheny et al., J Immunol 2000 : Furthermore, VCAM-1 ligand binding stimulated NADPH oxidase dependent production of ROS by the endothelial cells lines and primary endothelial cell cultures
Cook-Mills et al., Mol Immunol 2002 : VCAM-1 outside-in signals are mediated by NADPH oxidase production of reactive oxygen species and subsequently activation of matrix metalloproteinases
Cook-Mills et al., Biochem J 2004 (Calcium Signaling) : Addition of ionomycin overcame the calcium channel blocker suppression of VCAM-1 stimulated NADPH oxidase activity, but could not reverse the inhibitory effect imposed by intracellular calcium blockage, indicating that both intracellular and extracellular calcium mobilization are required for VCAM-1 mediated activation of NADPH oxidase ... Furthermore, VCAM-1 specifically activated the Rho-family GTPase Rac1, and VCAM-1 activation of NADPH oxidase was blocked by a dominant negative Rac1
Deem et al., Blood 2004 : VCAM-1 activates endothelial cell nicotinamide adenine dinucleotide phosphate ( NADPH ) oxidase in minutes, and this activity is required for VCAM-1 dependent lymphocyte migration ... The activation of endothelial cell MMPs required VCAM-1 stimulated endothelial cell NADPH oxidase activity as determined by scavenging of reactive oxygen species ( ROS ) and by pharmacologic or antisense inhibition of NADPH oxidase
Basta et al., Arterioscler Thromb Vasc Biol 2005 (Atherosclerosis) : The inhibition of NAD ( P ) H oxidase by apocynin and diphenylene iodonium, and of the mitochondrial electron transport system at complex II by thenoyltrifluoroacetone ( TTFA ), significantly inhibited both AGE induced ROS production and VCAM-1 expression, whereas these effects were potentiated by rotenone and antimycin A, specific inhibitors of mitochondrial complex I and III, respectively
Yamagishi et al., Int J Tissue React 2005 : These results demonstrate that minodronate could inhibit VCAM- 1 expression in AGE exposed ECs by suppressing NADPH oxidase derived ROS generation, probably via inhibition of geranylgeranylation of Rac, a component of endothelial NADPH oxidase
Abdala-Valencia et al., Am J Physiol Lung Cell Mol Physiol 2007 (Asthma...) : Ligation of VCAM-1 activates endothelial cell NADPH oxidase , which is required for VCAM-1 dependent leukocyte migration in vitro ... These data suggest that VCAM-1 induction of NADPH oxidase in the endothelium is necessary for the eosinophil recruitment during allergic inflammation
Cook-Mills et al., Cell Mol Biol Incl Cyto Enzymol 2006 : VCAM-1 activates endothelial cell NADPH oxidase followed by the generation of 1 microM H2O2
Carluccio et al., Am J Physiol Heart Circ Physiol 2007 (Hyperhomocysteinemia) : Homocysteine induces VCAM-1 gene expression through NF-kappaB and NAD ( P ) H oxidase activation : protective role of Mediterranean diet polyphenolic antioxidants
Song et al., Free Radic Biol Med 2011 (AIDS Dementia Complex) : Nox2 based NADPH oxidase mediates HIV-1 Tat induced up-regulation of VCAM-1/ICAM-1 and subsequent monocyte adhesion in human astrocytes ... HIV-1 Tat induced up-regulation of VCAM-1/ICAM-1 and subsequent increased adhesion of monocytes to astrocytes were blocked by a general NADPH oxidase inhibitor, diphenylene iodonium, and a specific inhibitor of NADPH oxidase assembly, 9R3A-gp91ds
Katsume et al., Arterioscler Thromb Vasc Biol 2011 (Aortic Diseases...) : Lysophosphatidylcholine activated PYK2 induced NADPH oxidase mediated ROS generation and ROS mediated synthesis of tumor necrosis factor-a (TNFa), vascular cell adhesion molecule-1 ( VCAM-1 ), monocyte chemotactic protein-1 (MCP-1), and p21Cip1/Ets-1
Abdala-Valencia et al., PloS one 2011 : VCAM-1 activation of endothelial cell NADPH oxidase/PKCa/PTP1B induces transient ERK1/2 activation that is necessary for VCAM-1 dependent leukocyte TEM
Peshavariya et al., PloS one 2013 (Inflammation) : Inhibition of NADPH oxidase activity by either dominant negative Rac1 ( N17Rac1 ) or DPI significantly attenuated TNFa induced ICAM-1and VCAM-1 expression