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AKT3 — ANGPT2
Text-mined interactions from Literome
Gorin et al., FASEB J 2001
:
We investigated the
effect of
Ang II on
Akt/PKB activity in MCs ...
Activation of
Akt/PKB by
Ang II was not abrogated by the PI3-K inhibitors or by the introduction of a dominant negative PI3-K, indicating that in MCs, PI3-K is not an upstream mediator of Akt/PKB activation by Ang II
Motley et al., Hypertension 2003
:
By immunoblotting with a phospho-specific antibody for Akt, we found that
Ang II inhibits insulin induced
Akt phosphorylation in a time- and concentration dependent manner
Benndorf et al., Circ Res 2003
:
We therefore investigated the
effect of
Ang II on VEGF induced
Akt and eNOS phosphorylation
Chiu et al., Am J Physiol Gastrointest Liver Physiol 2005
:
To elucidate the downstream targets of EGFR, we demonstrated that
ANG II stimulated phosphorylation of
Akt at Ser473, mTOR at Ser2448, p70S6K1 at Thr389, and S6 ribosomal protein at Ser ( 235/236 )
Izawa et al., Exp Cell Res 2005
(Hypertension...) :
Ang II inhibition of insulin stimulated IRS-1 tyrosyl phophorylation and
Akt activation were reversed by PD98059 but not by SP600125
Li et al., Am J Physiol Heart Circ Physiol 2005
(Carotid Artery Injuries) :
In cultured vascular smooth muscle cells,
ANG II activates
Akt through cytosolic phospholipase A2 (cPLA2) dependent phospholipase D2 (PLD2)
Benkirane et al., Am J Physiol Heart Circ Physiol 2006
:
15d-PGJ2 and rosiglitazone decreased ERK 1/2 and
Akt peak activity, both of which were
induced by
ANG II via the AT1 receptor
Hingtgen et al., Physiol Genomics 2006
(Hypertrophy) :
Finally,
ANG II caused a time dependent increase in
Akt activity via activation of AT(1) receptors, and this response was abolished by Ad-mediated expression of cytosolic human O2-* dismutase ( AdCu/ZnSOD )
Foo et al., J Cell Physiol 2006
(Hypertrophy) :
Adenoviral overexpression of HO-1 was accompanied by a significant increase in
Ang II induced phosphorylation of
Akt , however, Ang II-mediated p38 mitogen activated protein kinase ( MAPK ) phosphorylation was attenuated
Daly et al., Proc Natl Acad Sci U S A 2006
:
In addition, we show that
Ang-2 , like Ang-1,
activates Tie2/Akt signaling in vivo, thereby inhibiting the expression of FOXO1 target genes
Niu et al., Cancer Res 2007
(Breast Neoplasms...) :
Consistent with the important roles of AKT and mitogen activated protein kinase in the HER2 signaling pathway,
AKT and ERK mitogen activated protein kinase ( MAPK ) kinase activity is
necessary for
Ang-2 up-regulation by HER2
Kou et al., Vascul Pharmacol 2007
:
Low concentration
Ang II caused a dose dependent increase in
Akt phosphorylation, while high concentration of Ang II led to a decrease of Akt phosphorylation
Zhong et al., Br J Pharmacol 2008
(Insulin Resistance) :
In addition,
Ang II diminished insulin stimulated phosphorylation of
Akt ( at Ser ( 473 ) ) and eNOS ( at Ser ( 1177 ) ) and NO generation, effects which were reversed by ACE2 gene transfer and anti-MIF treatment in endothelial cells
Zhao et al., Acta Biochim Biophys Sin (Shanghai) 2008
(Breast Neoplasms) :
Ang II significantly
reduced the ratio of apoptotic cells and stimulation of
phospho-Akt-Thr308 and phospho-Akt-Ser473 in a dose dependent and time dependent manner
Tabet et al., Circ Res 2008
(Hypertension) :
Ang II stimulation
increased activation of ERK1/2, p38MAPK, and
AKT , with enhanced effects in SHR. SHP-2 knockdown resulted in increased AKT phosphorylation, without effect on ERK1/2 or p38MAPK
Chiou et al., Evidence-based complementary and alternative medicine : eCAM 2011
:
Western blot analysis revealed
Ang II increased the phosphorylation levels of
Akt and mitogen activated protein kinases ( MAPKs ; p38, ERK1/2 and JNK ) in rVSMC ... Also, the CQC pretreatment markedly suppressed
Ang-II induced phosphorylation of
Akt and JNK rather than ERK1/2, although it failed to affect p38 phosphorylation
Wang et al., Diabetologia 2010
(Diabetes Mellitus, Experimental...) :
Oxidative stress and formation of AGEs were assessed by immunoblotting, expression of
Ang-2 ( also known as Angpt2 ) by RT-PCR,
activation of protein kinase B (
AKT ) and heat shock protein (HSP)-27 levels by immunofluorescence, and incipient retinal vascular changes by quantitative morphometry of retinal digest preparations
Liu et al., Zhonghua Zheng Xing Wai Ke Za Zhi 2010
(Cicatrix, Hypertrophic) :
Ang II increased
Akt phosphorylation and PI3K activity in cultured hypertrophic scar fibroblasts in a dose- and time dependent manner
Zhao et al., J Cell Physiol 2010
(Breast Neoplasms) :
In addition,
Ang II caused rapid activation of
p-Akt in a dose- and time dependent manner
Schreiner et al., Cardiovasc Res 2011
:
Since NADPH oxidases (Nox) 1 and 4 are major ROS sources in VSMCs, we examined their need for
Akt phosphorylation in
response to
Ang II or EGF
Hua et al., American journal of physiology. Renal physiology 2012
:
In these studies, we determined that
ANG II induces phosphorylation of ETS-1 via activation of the type 1 ANG II receptor and that Erk1/2 and
Akt/PKB phosphorylation are
required for these effects
Chao et al., PloS one 2013
:
Furthermore,
Ang II stimulated ERK and
Akt phosphorylation in NSCs. Pretreatment of MEK inhibitor, but not PI3K inhibitor, inhibited Ang II-induced ERK phosphorylation as well as cell proliferation