PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28338195-5 2017 Autophagy inhibitor 3-MA could inhibit TGF-b1 upregulated autophagy. 3-methyladenine 20-24 transforming growth factor beta 1 Homo sapiens 39-45 34497522-13 2021 In addition, delayed administration of 3-MA was effective in reducing EMT induced by TGF-beta1. 3-methyladenine 39-43 transforming growth factor beta 1 Homo sapiens 85-94 32638014-9 2020 In addition, the inhibitory effects of ISL on TGF-beta1-induced fibrogenic features in MRC-5 cells were enhanced by pretreatment with autophagy activator Rapmycin and PI3K/AKT inhibitor LY294002 and reversed by autophagy inhibitor 3-methyladenine and PI3K/AKT activator IGF-1. 3-methyladenine 231-246 transforming growth factor beta 1 Homo sapiens 46-55 30293967-3 2018 In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-beta1 (TGF-beta1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. 3-methyladenine 66-81 transforming growth factor beta 1 Homo sapiens 190-222 30293967-3 2018 In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-beta1 (TGF-beta1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. 3-methyladenine 66-81 transforming growth factor beta 1 Homo sapiens 224-233 30293967-3 2018 In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-beta1 (TGF-beta1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. 3-methyladenine 83-87 transforming growth factor beta 1 Homo sapiens 190-222 30293967-3 2018 In the present study, we observed that inhibition of autophagy by 3-methyladenine (3-MA) abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-beta1 (TGF-beta1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. 3-methyladenine 83-87 transforming growth factor beta 1 Homo sapiens 224-233 29138833-11 2018 Finally, miR-16 mimics inhibited TGF-beta1-induced EMT, and this effect was attenuated by autophagy inhibitor 3-MA. 3-methyladenine 110-114 transforming growth factor beta 1 Homo sapiens 33-42 34847836-9 2022 The autophagy inhibitor 3-MA significantly suppressed TGFbeta1 expression and tube formation in EA.hy926 cells. 3-methyladenine 24-28 transforming growth factor beta 1 Homo sapiens 54-62 33741330-5 2021 Modulation of autophagy by rapamycin, 3-methyladenine or ATG-5 knockdown regulated the expression of CAFs markers, suggesting a role of autophagy in the tumor promotion mechanism of TGF-beta1-induced CAFs activation. 3-methyladenine 38-53 transforming growth factor beta 1 Homo sapiens 182-191 33741330-7 2021 We demonstrated that TGF-beta1-activated CAFs promote tumor invasion, pulmonary metastasis and EMT, which act through autophagy and overexpression of FAP-alpha in both models, while autophagy inhibitor 3-methyladenine blocked these effects induced by TGF-beta1-activated CAFs. 3-methyladenine 202-217 transforming growth factor beta 1 Homo sapiens 21-30 33741330-7 2021 We demonstrated that TGF-beta1-activated CAFs promote tumor invasion, pulmonary metastasis and EMT, which act through autophagy and overexpression of FAP-alpha in both models, while autophagy inhibitor 3-methyladenine blocked these effects induced by TGF-beta1-activated CAFs. 3-methyladenine 202-217 transforming growth factor beta 1 Homo sapiens 251-260 31450620-13 2019 Treatment with the autophagy inhibitor 3-MA resulted in a decrease of autophagy markers and collagen in the TGF-beta-treated fibroblasts. 3-methyladenine 39-43 transforming growth factor beta 1 Homo sapiens 108-116 30320898-9 2019 The inhibition of autophagy with CQ or 3MA also decreased the expression of TGF-beta1 and p-Smad3. 3-methyladenine 39-42 transforming growth factor beta 1 Homo sapiens 76-85 28678325-5 2017 Autophagy inhibitor 3-methyladenine (3-MA) could reverse TGF-beta1 induced autophagy process. 3-methyladenine 20-35 transforming growth factor beta 1 Homo sapiens 57-66 28678325-5 2017 Autophagy inhibitor 3-methyladenine (3-MA) could reverse TGF-beta1 induced autophagy process. 3-methyladenine 37-41 transforming growth factor beta 1 Homo sapiens 57-66 28678325-6 2017 Also, TGF-beta1 significantly promotes the invasion ability of HepG2 cells; however, this process could effectively reverse by autophagy inhibitor 3-MA. 3-methyladenine 147-151 transforming growth factor beta 1 Homo sapiens 6-15 22322529-11 2012 Similarly, when autophagy was prevented at an early stage by application of 3-methyladenine, the pro-apoptotic effects of TGF-beta1 were attenuated. 3-methyladenine 88-103 transforming growth factor beta 1 Homo sapiens 146-155