Gene interactions and pathways from curated databases and text-mining

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CAV2 — EPHB2

Text-mined interactions from Literome

Labrecque et al., Mol Biol Cell 2003 : Removal of caveolin and VEGFR-2 from caveolae by cholesterol depletion resulted in an increase in both basal and VEGF induced phosphorylation of VEGFR-2, but led to the inhibition of VEGF induced ERK activation and endothelial cell migration, suggesting that localization of VEGFR-2 to these domains is crucial for VEGF mediated signaling
Kawabe et al., Am J Physiol Heart Circ Physiol 2004 : Taken together, caveolin in caveolae may keep ERK inactive, but when caveolin is translocated to noncaveolar sites in response to stretch stress, caveolin mediates stretch induced ERK activation through an association with beta1-integrins/Fyn/Shc
Volonte et al., FASEB J 2005 : We also demonstrate that down-regulation of endogenous caveolin-1 expression activates ERK and that activation of the p42/44 MAP kinase pathway is necessary to promote muscle regeneration
Kim et al., Biochem Biophys Res Commun 2005 : Direct interaction between ERK and caveolin-2 was confirmed by immunoprecipitation and phosphorylated ERK increased the specific interaction in response to insulin
Oh et al., J Cell Biochem 2006 : However in contrast to adipocytes, phosphorylation of insulin receptor beta (IRbeta) and Akt/Erk was not affected by the respective downregulation of caveolin-1 or caveolin-3 in the muscle cells
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) : Adenovirally mediated expression of caveolin-1 in neurons from caveolin-1 ( -/- ) mice restored NMDA mediated enhancement of P-Src and P-ERK1/2 , redistributed NMDAR2B to buoyant fractions, and enhanced NMDAR2B localization to membrane rafts ... We conclude that caveolin-1 , perhaps via its ability to scaffold key signaling components, is essential for NMDAR localization to neuronal membrane rafts, NMDAR/Src tyrosine kinase family/ERK signaling, and protection of neurons from ischemic injury and cell death
Albinsson et al., Am J Physiol Cell Physiol 2008 (Hypertrophy...) : In conclusion, caveolin 1 contributes to low basal ERK1/2 and Akt activity and is required for Akt dependent signals in response to shear stress ( flow ) but is not essential for trophic effects of stretch ( pressure ) in the vascular wall
Thomas et al., Breast Cancer Res Treat 2010 (Breast Neoplasms) : The WT-MCF-7 cells showed abundant expression of caveolin-1 which potentiated oestrogen-receptor ( ERalpha ) signalling and promoted cell growth despite caveolin-1 mediating inhibition of ERK signalling ... Recombinant expression of caveolin-1 in TAM-R cells did not affect EGFR/ERK activity, potentially due to mislocalisation of caveolin-1 through hyperactivation of the mTOR pathway or altered caveolin-1 phosphorylation
Singh et al., Atherosclerosis 2011 (Atherosclerosis) : The effect of increased caveolin-1 expression on leptin dependent activation of ERK1/2 and eNOS was determined by Western blot analysis
Feng et al., J Cell Physiol 2012 : Downregulation of caveolin-1 significantly attenuated the FGF2 induced activation of AKT1 and ERK1/2 and inhibited FGF2 induced cell proliferation, migration and tube formation in oFPAE cells
Huang et al., FASEB J 2011 : Exposure to HIV-1 infected monocytes induced phosphorylation of ERK1/2 and Akt in hCMEC by 2.5- and 3.6-fold, respectively ; however, these effects were attenuated by overexpression of PPARa or PPAR? and by silencing of caveolin-1 ( cav-1 )
Watson et al., Steroids 2012 (MAP Kinase Signaling System...) : Estrogen- and xenoestrogen induced ERK signaling in pituitary tumor cells involves estrogen receptor-a interactions with G protein-ai and caveolin I