Gene interactions and pathways from curated databases and text-mining

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CAV2 — MAPK3

Text-mined interactions from Literome

Minelli et al., Peptides 2006 : It greatly enhances the phosphorylation of hsp27, alpha-B-crystallin, Cdc2, and p-38 MAPK , whereas it decreases the phosphorylation of MEK1, Cav 2 , GSK3a, PKB/Akt, PKCdelta, PKCgamma, and Erk2
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
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
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
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