PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22581458-6 2012 These protective effects of the GRK2 inhibitor may be attributable to the augmented Akt/eNOS pathway activation (as evidenced by increases in Akt phosphorylation at Ser(473) and at Thr(308), and eNOS phosphorylation at Ser(1177)) and to the prevention of the GRK2 translocation and promotion of beta-arrestin 2 translocation to the membrane under clonidine stimulation. Clonidine 347-356 thymoma viral proto-oncogene 1 Mus musculus 84-87 29463871-9 2018 At 21 days, clonidine withdrawal triggered rebound hypertension together with impaired endothelium-dependent relaxation, increased GRK2 activity, and reduced Akt/endothelial NO synthase (eNOS)/NO production in aortas. Clonidine 12-21 thymoma viral proto-oncogene 1 Mus musculus 158-161 29463871-10 2018 Conversely, withdrawal of the combination clonidine/GRK2-inhibitor treatment did not cause rebound hypertension, and normal induction of endothelium-dependent relaxation, decreased GRK2 activity, and increased Akt/eNOS were observed in aortas from DM mice. Clonidine 42-51 thymoma viral proto-oncogene 1 Mus musculus 210-213 26632178-0 2015 Resveratrol Ameliorates Clonidine-Induced Endothelium-Dependent Relaxation Involving Akt and Endothelial Nitric Oxide Synthase Regulation in Type 2 Diabetic Mice. Clonidine 24-33 thymoma viral proto-oncogene 1 Mus musculus 85-88 26632178-11 2015 Interestingly, the phosphorylation of Akt and eNOS was increased under stimulation with RV and clonidine only in diabetic mice. Clonidine 95-104 thymoma viral proto-oncogene 1 Mus musculus 38-41 26632178-12 2015 Thus, either RV or clonidine causes Akt-dependent NO-mediated relaxation, which is weaker in diabetic mice than controls. Clonidine 19-28 thymoma viral proto-oncogene 1 Mus musculus 36-39 26632178-13 2015 However, additional exposure to RV and clonidine has an augmenting effect on the Akt/eNOS signaling pathway under diabetic conditions. Clonidine 39-48 thymoma viral proto-oncogene 1 Mus musculus 81-84 26632178-14 2015 RV-induced Akt/eNOS activity may be a common link involved in the clonidine-induced Akt/eNOS activity, so RV and clonidine may have a synergistic effect. Clonidine 66-75 thymoma viral proto-oncogene 1 Mus musculus 11-14 26632178-14 2015 RV-induced Akt/eNOS activity may be a common link involved in the clonidine-induced Akt/eNOS activity, so RV and clonidine may have a synergistic effect. Clonidine 66-75 thymoma viral proto-oncogene 1 Mus musculus 84-87 26632178-14 2015 RV-induced Akt/eNOS activity may be a common link involved in the clonidine-induced Akt/eNOS activity, so RV and clonidine may have a synergistic effect. Clonidine 113-122 thymoma viral proto-oncogene 1 Mus musculus 11-14 26632178-14 2015 RV-induced Akt/eNOS activity may be a common link involved in the clonidine-induced Akt/eNOS activity, so RV and clonidine may have a synergistic effect. Clonidine 113-122 thymoma viral proto-oncogene 1 Mus musculus 84-87 22925038-12 2013 CONCLUSION: GRK2 plays a key role in modulating the aortic vasodilator effect of clonidine by selectively affecting the Akt/eNOS pathway. Clonidine 81-90 thymoma viral proto-oncogene 1 Mus musculus 120-123 22581458-8 2012 Our work provides the first evidence that in diabetes, the GRK2 inhibitor ameliorates vascular endothelial dysfunction via the Akt/eNOS pathway by inhibiting GRK2 activity and enhancing beta-arrestin 2 translocation under clonidine stimulation, thereby contributing to a blood pressure-lowering effect. Clonidine 222-231 thymoma viral proto-oncogene 1 Mus musculus 127-130 19721331-6 2009 In control aortas (from males or females), the clonidine-induced relaxation was abolished by Akt-inhibitor treatment. Clonidine 47-56 thymoma viral proto-oncogene 1 Mus musculus 93-96 21571071-10 2011 Akt phosphorylation was markedly below control in the clonidine-stimulated diabetes. Clonidine 54-63 thymoma viral proto-oncogene 1 Mus musculus 0-3 21571071-11 2011 The phosphorylation of Akt at Thr308 was significantly normalized and the phosphorylation of eNOS at Ser1177 tended to be increased by GRK2-inhibitor in the clonidine-stimulated diabetics. Clonidine 157-166 thymoma viral proto-oncogene 1 Mus musculus 23-26 18391484-7 2008 The expression levels of both total Akt protein and clonidine-induced Ser-473-phosphorylated Akt were significantly decreased in diabetic aortas, while chronic simvastatin administration improved these decreased levels. Clonidine 52-61 thymoma viral proto-oncogene 1 Mus musculus 93-96 15505117-2 2004 We investigated the involvement of the PI3-K/Akt pathway in the relaxation responses to acetylcholine (ACh) and clonidine in a new type 2 diabetic model (streptozotocin plus nicotinamide-induced diabetic mice). Clonidine 112-121 thymoma viral proto-oncogene 1 Mus musculus 45-48 15505117-5 2004 In control mice, the clonidine-induced and insulin-induced relaxations were each abolished by LY294002 and by Wortmannin (inhibitors of PI3-K), and also by Akt-inhibitor treatment. Clonidine 21-30 thymoma viral proto-oncogene 1 Mus musculus 156-159 15505117-8 2004 The clonidine-induced Ser-473 phosphorylation of Akt through PI3-K was significantly decreased in our model; however, that induced by ACh was not. Clonidine 4-13 thymoma viral proto-oncogene 1 Mus musculus 49-52