Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK7

CAV1 — MAPK7

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
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
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
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