PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23714396-10 2013 The present study demonstrates testosterone administration improves hypertrophy in myoblasts that basally display impaired differentiation and hypertrophic capacity vs. their parental controls, the action of testosterone in this model was mediated by PI3K/Akt pathway. Testosterone 31-43 thymoma viral proto-oncogene 1 Mus musculus 256-259 23714396-10 2013 The present study demonstrates testosterone administration improves hypertrophy in myoblasts that basally display impaired differentiation and hypertrophic capacity vs. their parental controls, the action of testosterone in this model was mediated by PI3K/Akt pathway. Testosterone 208-220 thymoma viral proto-oncogene 1 Mus musculus 256-259 23116773-0 2013 Testosterone regulation of Akt/mTORC1/FoxO3a signaling in skeletal muscle. Testosterone 0-12 thymoma viral proto-oncogene 1 Mus musculus 27-30 23116773-3 2013 However, the testosterone sensitivity of Akt/mTOR signaling requires further understanding in order to grasp the significance of varied testosterone levels seen with wasting disease on muscle protein turnover regulation. Testosterone 13-25 thymoma viral proto-oncogene 1 Mus musculus 41-44 23116773-11 2013 Testosterone (T) sensitivity of Akt/mTORC1 signaling was examined in C(2)C(12) myotubes, and mTOR phosphorylation was induced independent of Akt activation at low T concentrations, while a higher T concentration was required to activate Akt signaling. Testosterone 0-12 thymoma viral proto-oncogene 1 Mus musculus 32-35 23116773-14 2013 Acute Akt activation in C(2)C(12) myotubes is sensitive to a high concentration of testosterone, and low concentrations of testosterone can activate mTOR signaling independent of Akt. Testosterone 83-95 thymoma viral proto-oncogene 1 Mus musculus 6-9 23116773-14 2013 Acute Akt activation in C(2)C(12) myotubes is sensitive to a high concentration of testosterone, and low concentrations of testosterone can activate mTOR signaling independent of Akt. Testosterone 123-135 thymoma viral proto-oncogene 1 Mus musculus 179-182 20501642-9 2010 In cardiac myoblast cells, testosterone up-regulated Akt phosphorylation and Tfam expression and exerted an antiapoptotic effect against Dox-induced cardiotoxicity. Testosterone 27-39 thymoma viral proto-oncogene 1 Mus musculus 53-56 22405892-0 2012 Testosterone up-regulates seladin-1 expression by iAR and PI3-K/Akt signaling pathway in C6 cells. Testosterone 0-12 thymoma viral proto-oncogene 1 Mus musculus 64-67 22405892-4 2012 Furthermore, we found that testosterone significantly increased the phosphorylation level of V-akt murine thymoma viral oncogene (Akt), a key effector of the phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway, while a specific PI3-K inhibitor LY294002 obviously prevented the activation of Akt phosphorylation. Testosterone 27-39 thymoma viral proto-oncogene 1 Mus musculus 95-98 22405892-4 2012 Furthermore, we found that testosterone significantly increased the phosphorylation level of V-akt murine thymoma viral oncogene (Akt), a key effector of the phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway, while a specific PI3-K inhibitor LY294002 obviously prevented the activation of Akt phosphorylation. Testosterone 27-39 thymoma viral proto-oncogene 1 Mus musculus 130-133 22405892-4 2012 Furthermore, we found that testosterone significantly increased the phosphorylation level of V-akt murine thymoma viral oncogene (Akt), a key effector of the phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway, while a specific PI3-K inhibitor LY294002 obviously prevented the activation of Akt phosphorylation. Testosterone 27-39 thymoma viral proto-oncogene 1 Mus musculus 192-195 22405892-4 2012 Furthermore, we found that testosterone significantly increased the phosphorylation level of V-akt murine thymoma viral oncogene (Akt), a key effector of the phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway, while a specific PI3-K inhibitor LY294002 obviously prevented the activation of Akt phosphorylation. Testosterone 27-39 thymoma viral proto-oncogene 1 Mus musculus 192-195 20403060-7 2011 The observed positive regulation of atrogin-1 (Fbxo32) by testosterone could be explained by the phosphorylation of Akt and Foxo3a, as determined by Western blotting. Testosterone 58-70 thymoma viral proto-oncogene 1 Mus musculus 116-119 21045173-5 2011 Orchidectomy also suppressed the IGF-I/Akt pathway, activated the atrophy-inducing E3 ligases MuRF1 and MAFBx, and suppressed several energy metabolism pathways, and all of these effects were reversed by testosterone replacement. Testosterone 204-216 thymoma viral proto-oncogene 1 Mus musculus 39-42 35452821-5 2022 Mechanistically, DAB2IP could dramatically inhibit the AKR1C3 promoter activity and the conversion from androgen precursors (i.e., DHEA) to testosterone through PI3K/AKT/mTOR/ETS1 signaling. Testosterone 140-152 thymoma viral proto-oncogene 1 Mus musculus 166-169 20032061-4 2010 We demonstrated that the number of primary follicles was increased after 10 d culture with testosterone treatment via phosphatidylinositol 3-kinase/Akt pathway. Testosterone 91-103 thymoma viral proto-oncogene 1 Mus musculus 148-151 18953857-7 2008 The phosphorylation levels of InsR, Akt, and GSK3Pbeta were significantly down-regulated by adding of testosterone at the concentration of 10(-6) mol/L for 3-30 minutes (all P < 0.05) or by adding of testosterone at the concentrations of 10(-7) - 10(-6) mol/L for 24 hours (all P < 0.05). Testosterone 102-114 thymoma viral proto-oncogene 1 Mus musculus 36-39 15177002-11 2004 Western blot analysis showed that DHT, 17beta-estradiol, and testosterone (T) induce a rapid and transient phosphorylation of Akt in MC3T3-E1 cells. Testosterone 61-73 thymoma viral proto-oncogene 1 Mus musculus 126-129 31693697-9 2019 Testosterone supplementation inhibited GSK3alpha in the myocytes in a PI3K/AKT pathway dependent manner; on the other hand GSK3beta gene expression was reduced in the skeletal muscle upon testosterone supplementation. Testosterone 0-12 thymoma viral proto-oncogene 1 Mus musculus 75-78 32717722-9 2020 Furthermore, we uncover the underlying molecular mechanism and show that testosterone treatment restored the phosphorylation of Akt and FoxO1a. Testosterone 73-85 thymoma viral proto-oncogene 1 Mus musculus 128-131 31693697-7 2019 We demonstrate that, in males, testosterone improves skeletal muscle insulin responsiveness by potentiating the PI3K-AKT pathway. Testosterone 31-43 thymoma viral proto-oncogene 1 Mus musculus 117-120 31693697-8 2019 The testosterone treated animals showed significant increase in the skeletal muscle Insulin Receptor (IR), p85 subunit of PI3K, P-GSK3alpha (Ser-21), and P-AKT (Ser-473) levels as compared to the control animals; but there was no significant change in total AKT and GSK3alpha. Testosterone 4-16 thymoma viral proto-oncogene 1 Mus musculus 156-159 31693697-8 2019 The testosterone treated animals showed significant increase in the skeletal muscle Insulin Receptor (IR), p85 subunit of PI3K, P-GSK3alpha (Ser-21), and P-AKT (Ser-473) levels as compared to the control animals; but there was no significant change in total AKT and GSK3alpha. Testosterone 4-16 thymoma viral proto-oncogene 1 Mus musculus 258-261 32046379-8 2020 Insulin augmented testosterone induced estradiol generation through activation of the AKT pathway. Testosterone 18-30 thymoma viral proto-oncogene 1 Mus musculus 86-89 28854419-11 2017 CONCLUSION: Findings suggested that the membrane association of AR was mediated by the MEK and Akt phosphorylation signaling pathways, which resulted in Src activation and was initiated by testosterone binding to the membrane-localized AR. Testosterone 189-201 thymoma viral proto-oncogene 1 Mus musculus 95-98 29145710-8 2018 Testosterone treatment reduced (p < 0.05) prolonged detumescence in Sickle mice and normalized downregulated P-PDE5 (Ser-92), PDE5, P-eNOS (Ser-1177), and P-Akt (Ser-473) protein expressions in the Sickle mouse penis. Testosterone 0-12 thymoma viral proto-oncogene 1 Mus musculus 160-163 28642037-5 2017 Cellular signaling studies indicate that testosterone regulates macrophage polarization through the inhibitory regulative G-protein (Galphai) mainly, rather than via androgen receptors, and phosphorylation of Akt. Testosterone 41-53 thymoma viral proto-oncogene 1 Mus musculus 209-212 28642037-9 2017 Therefore, our findings indicate that testosterone inhibits pre-adipocyte differentiation by switching macrophages to M2 polarization through the Galphai and Akt signaling pathways. Testosterone 38-50 thymoma viral proto-oncogene 1 Mus musculus 158-161 26538344-1 2016 We have previously highlighted the ability of testosterone (T) to improve differentiation and myotube hypertrophy in fusion impaired myoblasts that display reduced myotube hypertrophy via multiple population doublings (PD) versus their parental controls (CON); an observation which is abrogated via PI3K/Akt inhibition (Deane et al. Testosterone 46-58 thymoma viral proto-oncogene 1 Mus musculus 304-307 26538344-13 2016 In conclusion, testosterones ability to improve differentiation and myotube hypertrophy occurred predominately via increases in AR and Akt abundance in both CON and PD cells, with fusion impaired cells (PD) showing an increased responsiveness to T induced AR levels. Testosterone 15-28 thymoma viral proto-oncogene 1 Mus musculus 135-138 27941939-5 2016 However, testosterone treatment inactivated GSK3alpha independent of PI3K/AKT pathway and inhibited FOXO1 By interaction of androgen receptor to FOXO1 and downregulated PEPCK, causing repression of gluconeogenic pathway, which is otherwise upregulated in T2DM, resulted in better glucose homeostasis. Testosterone 9-21 thymoma viral proto-oncogene 1 Mus musculus 74-77