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ATP5O — EPHB2
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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