PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26487003-2 2015 Our previous work shows that 2-ME inhibits initiation (blocks phosphorylation of ERK and Akt) and progression (reduces cyclin expression and increases expression of cyclin inhibitors) of the mitogenic pathway and interferes with mitosis (disrupts tubulin organization). 2-Methoxyestradiol 29-33 mitogen-activated protein kinase 1 Homo sapiens 81-84 17012370-0 2007 Involvement of microtubules, p38, and Rho kinases pathway in 2-methoxyestradiol-induced lung vascular barrier dysfunction. 2-Methoxyestradiol 61-79 mitogen-activated protein kinase 1 Homo sapiens 29-32 17012370-12 2007 Together, these results indicate that 2ME-induced barrier disruption is governed by MT depolymerization and p38- and ROCK-dependent mechanisms. 2-Methoxyestradiol 38-41 mitogen-activated protein kinase 1 Homo sapiens 108-111 14694442-6 2004 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol 38-42 mitogen-activated protein kinase 1 Homo sapiens 51-88 14694442-6 2004 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol 38-42 mitogen-activated protein kinase 1 Homo sapiens 90-93 14694442-6 2004 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol 170-174 mitogen-activated protein kinase 1 Homo sapiens 51-88 14694442-6 2004 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol 170-174 mitogen-activated protein kinase 1 Homo sapiens 90-93 14694442-7 2004 Taken together, the present findings indicate that 2-ME suppresses NF-kappaB/FLIP signaling and enhances DISC formation through inhibition of Akt, and that PC3 cells thereby are being sensitized to Fas-mediated apoptosis and by a process closely associated with ERK. 2-Methoxyestradiol 51-55 mitogen-activated protein kinase 1 Homo sapiens 262-265 21769948-0 2012 2-Methoxyestradiol induced Bax phosphorylation and apoptosis in human retinoblastoma cells via p38 MAPK activation. 2-Methoxyestradiol 0-18 mitogen-activated protein kinase 1 Homo sapiens 99-103 19883629-0 2010 2-Methoxyestradiol induces endoreduplication through the induction of mitochondrial oxidative stress and the activation of MAPK signaling pathways. 2-Methoxyestradiol 0-18 mitogen-activated protein kinase 1 Homo sapiens 123-127 18521846-4 2009 We found that 2-methoxyestradiol induced the activation of JNK, ERK, and p38 MAPKs. 2-Methoxyestradiol 14-32 mitogen-activated protein kinase 1 Homo sapiens 64-67 18521846-6 2009 In comparison, 2-methoxyestradiol-induced activation of ERK and p38 in these cells was found to have a protective effect against 2-MeO-E(2)-induced apoptosis. 2-Methoxyestradiol 15-33 mitogen-activated protein kinase 1 Homo sapiens 56-59 18521846-6 2009 In comparison, 2-methoxyestradiol-induced activation of ERK and p38 in these cells was found to have a protective effect against 2-MeO-E(2)-induced apoptosis. 2-Methoxyestradiol 129-139 mitogen-activated protein kinase 1 Homo sapiens 56-59 18521846-7 2009 Consistent with this observation, the presence of pharmacological inhibitor of ERK or p38 enhanced 2-methoxyestradiol-induced apoptosis. 2-Methoxyestradiol 99-117 mitogen-activated protein kinase 1 Homo sapiens 79-82 18521846-8 2009 Mechanistically, inhibition of ERK and p38 activity was associated with activation of various caspases and PARP cleavage, and it also stabilized the pro-apoptotic proteins Bax and Bim, thereby preventing them from degradation during 2-methoxyestradiol treatment. 2-Methoxyestradiol 233-251 mitogen-activated protein kinase 1 Homo sapiens 31-34 18521846-9 2009 These results suggest that ERK and p38 MAPKs may serve as viable targets for the sensitization of human breast cancer cells to 2-methoxyestradiol-induced apoptosis. 2-Methoxyestradiol 127-145 mitogen-activated protein kinase 1 Homo sapiens 27-30