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ATP5O — EPHB2

Text-mined interactions from Literome

Guerrero et al., Am J Physiol Lung Cell Mol Physiol 2001 : Dopamine regulates Na-K-ATPase in alveolar epithelial cells via MAPK-ERK dependent mechanisms
Kreydiyyeh et al., Pflugers Arch 2004 : Exogenous PGE ( 2 ) reduced protein expression of the ATPase within 15 min, even in presence of an ERK inhibitor
Al-Khalili et al., J Biol Chem 2004 : Insulin action on Na ( + ), K ( + ) -ATPase was dependent on ERK1/2 in HSMCs. Sequence analysis of Na ( + ), K ( + ) -ATPase alpha-subunits revealed several potential ERK phosphorylation sites
Zhong et al., Cell Mol Life Sci 2004 : C-peptide action on Na ( + ), K ( + ) -ATPase was ERK1/2 dependent in HRTCs. C-peptide stimulated Na ( + ), K ( + ) -ATPase activation, phosphorylation of alpha ( 1 ) -subunit and translocation of alpha ( 1 ) and beta ( 1 ) subunits to the BLM were abolished by a MEK1/2 inhibitor ( 20 muM PD98059 )
Bełtowski et al., Peptides 2006 : H2O2 and Src dependent transactivation of the EGF receptor mediates the stimulatory effect of leptin on renal ERK and Na+, K+-ATPase ... We conclude that leptin induced stimulation of renal Na ( + ), K ( + ) -ATPase involves H ( 2 ) O ( 2 ) generation, Src kinase, transactivation of the EGF receptor, and stimulation of ERK
Liu et al., Cell Mol Biol Incl Cyto Enzymol 2006 (Ion Channel Gating) : Therapeutic concentrations of digitalis drugs inhibit the proliferation of breast cancer cells by inducing the interaction of Na+/K+-ATPase with Src/EGFR, activation of ERK1/2 , and the resulting upregulation of cell cycle inhibitor p21Cip1
Lei et al., Am J Physiol Lung Cell Mol Physiol 2008 : These data indicate that activation of MAPK-ERK1/2 was required for the T3-induced increase in Na-K-ATPase activity in addition to the requirement for the PI3K pathway
Khundmiri et al., American journal of physiology. Renal physiology 2008 : PTH mediated regulation of Na+-K+-ATPase requires Src kinase dependent ERK phosphorylation
Soltoff et al., Am J Physiol Cell Physiol 2008 : Regulation of ERK1/2 by ouabain and Na-K-ATPase dependent energy utilization and AMPK activation in parotid acinar cells
Lei et al., Am J Physiol Lung Cell Mol Physiol 2011 : Inhibitors of Src kinase ( PP1 ), PI3K ( wortmannin ), and ERK1/2 ( U0126 ) all blocked the T3-induced Na-K-ATPase activity