◀ Back to EPHB2
AGTR2 — EPHB2
Text-mined interactions from Literome
Lehtonen et al., Mol Endocrinol 1999
:
Alanine substitutions further demonstrated that lysine 240, asparagine 242, and serine 243 are key residues for
AT2 induced apoptosis,
ERK inhibition, and SHP-1 activation ... To examine whether a functional link exists between activation of SHP-1 and apoptosis, we used a catalytically inactive SHP-1 mutant and demonstrated that preventing SHP-1 activation strongly attenuates
AT2 induced
ERK inhibition and apoptosis
Shibasaki et al., Hypertension 2001
:
Maximal
ERK activity induced by Ang II was
increased 1.9- and 2.2-fold by
AT(2) inhibition, which was abolished by orthovanadate but not okadaic acid or pertussis toxin ... Stable overexpression of SHP-1-dominant negative mutant completely abolished
AT(2) mediated inhibition of EGFR and
ERK activation ... These findings suggested that
AT(2) inhibits
ERK activity by inducing SHP-1 activity, leading to decreases in AP-1 activity and AP-1 regulated gene expression, in which EGFR dephosphorylation plays an important role via association of SHP-1
Takahashi et al., Eur J Clin Invest 2004
(Cardiomegaly...) :
These data suggest that PKC and
ERK1/2 are
activated by an
angiotensin II receptor mediated pathway and might play an important role in the progression of cardiac hypertrophy in renal failure
Ahn et al., J Biol Chem 2004
:
Differential kinetic and spatial patterns of beta-arrestin and G protein mediated
ERK activation by the
angiotensin II receptor
Chow et al., Prostate 2008
(Prostatic Neoplasms) :
Functional
AT(2)-receptors together with Ang II were identified in both cell lines and stimulation of these receptors
inhibited EGF induced DNA synthesis and
ERK2 phosphorylation
Yamada et al., Life Sci 1998
:
Moreover we observed that AT1 receptor stimulation activated extracellular signal regulated kinase ( ERK ), whereas the
AT2 receptor stimulation
inhibited the activation of
ERK