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ANGPT2 — SRC

Text-mined interactions from Literome

Touyz et al., J Hypertens 2001 (Calcium Signaling) : Ang II rapidly increased VSMC c-Src activity, with peak responses obtained at 1 min. Ang II induced a biphasic [ Ca2+ ] i response ( Emax = 636 +/- 123 nmol/l )
Ushio-Fukai et al., Arterioscler Thromb Vasc Biol 2001 : Although antioxidants had no effects on the Ca ( 2+ ) mobilization or phosphorylation of Ca ( 2+ ) -dependent tyrosine kinase Pyk2, they inhibited c-Src activation by Ang II , suggesting that c-Src is 1 signaling molecule that links ROS and EGF-R phosphorylation
Yoshizumi et al., Mol Pharmacol 2001 : Ang II caused a rapid tyrosine phosphorylation of Src homology and collagen (Shc) , which was inhibited by quercetin
Seta et al., J Biol Chem 2002 : Ang II activates ERKs via a Src-Ras dependent mechanism in AT1a-i2m ... In summary, while Src and ERKs are activated by Ang II even without heterotrimeric G protein coupling, the carboxyl terminus of the AT1 receptor is required for activation of Src
Shah et al., Mol Pharmacol 2002 : Ang II increased the association of Pyk2 with Src and with the epidermal growth factor receptor (EGF-R) ... Ang II-induced ERK activation in C9 cells is initiated by a PKCdelta dependent but Ca ( 2+ ) -independent mechanism and is mediated by the Src/Pyk2 complex through trans-activation of the EGF-R
Seshiah et al., Circ Res 2002 : These results suggest that c-Src , EGF receptor transactivation, phosphatidylinositol-3-kinase, and Rac play important roles in the sustained Ang II-mediated activation of vascular smooth muscle cell NAD ( P ) H oxidases and provide insight into the integrated signaling mechanisms whereby Ang II stimulation leads to activation of the growth related NAD ( P ) H oxidases
Espiritu et al., American journal of physiology. Renal physiology 2002 (Acidosis) : Regulation of renal Na-HCO cotransporter ( NBC1 ) activity by cholinergic agonists, ANG II , and acute acidosis ( CO ( 2 ) ) requires both Src family kinase (SFK) and classic MAPK pathway activation
Xiang et al., Zhejiang Da Xue Xue Bao Yi Xue Ban 2003 : To further clarify the mechanism of Ang II-induced intracellular signal transduction in vascular smooth muscle cells ( VSMCs ) proliferation by observing the effect of c-Src on Ang II-mediated MAPK activation and c-fos protein expressions in rat VSMCs ... Ang II can induce c-Src activation and intracellular signal transduction in VSMC which depend on c-Src activation, indicating that c-Src is a pivotal signal factor in VSMC proliferation
Godeny et al., Am J Physiol Cell Physiol 2006 : A loss of c-Src/Yes/Fyn blocked ANG II-dependent RSK2 activation, RSK2 nuclear translocation, serum-response factor (SRF) phosphorylation, a portion of c-fos transcriptional activity and c-Fos phosphorylation
Mima et al., Lab Invest 2006 (Diabetes Mellitus, Experimental...) : Ang II induced Col4 synthesis and increased expression of phospho-Src and phospho-Smad1 in cultured mesangial cells, which was blocked by olmesartan
Li et al., Am J Physiol Cell Physiol 2007 (MAP Kinase Signaling System) : Transfection of PAECs with G alpha ( i3 ) dominant negative ( DN ) cDNA blocked the ANG II-dependent activation of Src , ERK1/ERK2 phosphorylation, and increase in NOS expression
Yogi et al., Arterioscler Thromb Vasc Biol 2007 (MAP Kinase Signaling System) : Ang II but not ET-1 induced c-Src phosphorylation in c-Src ( +/+ ) VSMCs. Activation of c-Raf, an effector of Ras, was significantly increased by ET-1 and Ang II in c-Src ( +/+ ) VSMCs. Ang II but not ET-1 mediated c-Raf phosphorylation was inhibited by c-Src deficiency
Sampaio et al., Hypertension 2007 : Ang II significantly increased activation of c-Src , ERK1/2, and NAD ( P ) H oxidase and reduced phosphorylation of SHP-2 ( P < 0.05 ) in human endothelial cells
Montezano et al., Arterioscler Thromb Vasc Biol 2008 : Aldo and Ang II costimulation induced c-Src dependent activation of NAD ( P ) H oxidase and c-Src independent activation of ERK1/2 ( P < 0.05 ), without effect on ERK5, p38MAPK, or JNK
Block et al., J Biol Chem 2008 (Fibrosis...) : Small interfering RNA for Nox4 also inhibits Ang II-induced activation of Src and PDK-1 tyrosine phosphorylation ( total and on residues 9 and 373/376 ), demonstrating that Nox4 functions upstream of Src and PDK-1 ... This work provides the first evidence that Nox4 derived ROS are responsible for Ang II-induced PDK-1 tyrosine phosphorylation and activation through stimulation of Src
Touyz et al., Methods Mol Med 2001 : The Gß? subunits as well as their associated Ga ( 12 ) subunits, mediate Ang II-induced PLD activation via Src dependent mechanisms in vascular smooth muscle cells
Chen et al., J Am Soc Nephrol 2012 (Fibrosis) : Persistent activation of the Ang II receptor stimulated ROS dependent phosphorylation of Src , leading to sustained EGFR dependent signaling for TGFß expression
Ishida et al., Circ Res 1998 : Recently, we showed that Ang II activated c-Src , a nonreceptor kinase, which is a candidate to mediate Ang II signal events ... To determine whether c-Src is required for ERK1/2 activation by Ang II , we studied the effects of Src family-selective tyrosine kinase inhibitors on ERK1/2 activation and also studied Ang II-mediated signal events in Src-deficient and Src overexpressing VSMCs
Eguchi et al., J Biol Chem 1998 : Moreover, Ang II induced association of EGF receptor with catalytically active c-Src
Ushio-Fukai et al., Mol Pharmacol 1999 : This effect may be mediated by pp60(c-src) , because in beta-adrenergic receptor kinase1 overexpressing cells, pp60(c-src) activation was inhibited, and in normal cells anti-pp60(c-src) antibody inhibited Ang II-stimulated PLD activity