We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to NOS2

APOE — NOS2

Text-mined interactions from Literome

Ishigami et al., Arterioscler Thromb Vasc Biol 2000 : Reverse transcription-polymerase chain reaction amplification of RNA obtained from control and apoE treated SMCs demonstrated a direct role of apoE in activating inducible nitric oxide synthase (iNOS) gene expression
Guo et al., J Mol Neurosci 2004 (Alzheimer Disease...) : Apolipoprotein E3 (apoE3) and apoE4 suppressed oligomeric Abeta induced production of inducible nitric oxide synthase and cyclo-oxygenase-2, supporting an anti- inflammatory role for apoE
Hui et al., Neurobiol Aging 2005 : apoE inhibition of cell proliferation is mediated by its binding to proteoglycans and the resulting activation of inducible nitric oxide synthase
Moore et al., J Lipid Res 2005 (Carotid Artery Injuries...) : Apolipoprotein E inhibition of vascular hyperplasia and neointima formation requires inducible nitric oxide synthase ... Previous studies have shown apolipoprotein E (apoE) recruitment to medial layers of carotid arteries after vascular injury in vivo and apoE activation of inducible nitric oxide synthase (iNOS) in smooth muscle cells in vitro ... In contrast, overexpression of apoE in FVB/N mice activated iNOS expression in the injured vessels, resulting in protection against neointimal hyperplasia ... Thus, injury induced activation of iNOS requires apoE recruitment ... Moreover, both apoE and iNOS are necessary for the suppression of cell proliferation, and apoE recruitment without iNOS expression resulted in medial hyperplasia without cell migration to the intima
Kawamura et al., Arterioscler Thromb Vasc Biol 2007 (Atherosclerosis) : IL-1beta induced expression and activation of inducible nitric oxide synthase and cyclooxygenase-2 were inhibited by apoE in vascular smooth muscle cells ( VSMCs )