Gene interactions and pathways from curated databases and text-mining

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CAV1 — MAPK3

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Wang et al., Am J Respir Cell Mol Biol 2006 (Inflammation) : p38 mitogen activated protein kinase ( MAPK ) phosphorylation was increased by overexpressing caveolin-1 in RAW264.7 cells, whereas c-Jun N-terminal kinase, extracellular signal regulated kinase MAPK, and Akt phosphorylation were inhibited
Cabrita et al., J Biol Chem 2006 : Moreover, we demonstrate that the various Sprouty isoforms differ dramatically in their cooperation with Caveolin-1 mediated inhibition of mitogen activated protein kinase activation and that such cooperation is also highly dependent on the type of growth factor investigated and on cell density
Wang et al., Am J Pathol 2007 : Therefore, human immunodeficiency virus protease inhibitor ritonavir significantly inhibits cholesterol efflux from macrophages, which may be mediated by mitochondrial dysfunction, oxidative stress, ERK1/2 activation , and down-regulation of scavenger receptor B1 and caveolin-1
Head et al., FASEB J 2008 (Brain Ischemia) : Caveolin-1 expression is essential for N-methyl-D-aspartate receptor mediated Src and extracellular signal regulated kinase 1/2 activation and protection of primary neurons from ischemic cell death
Bianco et al., Am J Pathol 2008 (Neoplasm Invasiveness) : Furthermore, coexpression of Cav-1 together with Cr-1 in EpH4 Cr-1/Cav-1 cells inhibited Cr-1 mediated activation of c-src and mitogen activated protein kinase signaling pathways
Chen et al., Oncogene 2009 (Neoplasm Invasiveness...) : Further study revealed that the upregulation of caveolin-1 and inhibition of tumor cell invasion were mediated by reactive oxygen species induced p38 MAPK activation
Wu et al., J Cell Biochem 2009 : The increase in caveolin-1 expression was dependent on phosphorylation of the mitogen activated protein kinases ( MAPKs ) extracellular signal regulated kinase1/2 ( ERK1/2 ), p38, and Jun N-terminal kinase (JNK) and the transcriptional activation and translocation of nuclear factor- ? B ( NF-kappaB )
Lv et al., Inflamm Res 2010 (Inflammation) : Over-expression of caveolin-1 not only increased the production of pro-inflammatory cytokine TNF-alpha and IL-6, but also enhanced the expression of the cPLA2, p38 MAPK , and NF-kappaB
Lee et al., J Cell Physiol 2011 : Inhibition of p38 MAPK blocked high glucose induced Cav-1 and fibronectin ( FN ) expression
Chi et al., Future Microbiol 2011 (Disease Models, Animal...) : Furthermore, E44 invasion, E44/nicotine induced activation of Erk1/2 and clustering of a7 nAChR and caveolin-1 was specifically blocked by both siRNAs
Jagielska et al., Arterioscler Thromb Vasc Biol 2012 (Disease Models, Animal...) : Accordingly, cellular cholesterol depletion ( cyclodextrin ) and silencing of caveolin-1 ( small interfering RNA ) inhibited IL-1ß induced activation of p38-MAPK and MK2, as well as IL-1ß induced tube formation and migration