PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26083398-0 2015 Methotrexate Promotes Platelet Apoptosis via JNK-Mediated Mitochondrial Damage: Alleviation by N-Acetylcysteine and N-Acetylcysteine Amide. Methotrexate 0-12 mitogen-activated protein kinase 8 Homo sapiens 45-48 26083398-4 2015 MTX (10 muM) induced activation of pro-apoptotic proteins Bid, Bax and Bad through JNK phosphorylation leading to DeltaPsim dissipation, cytochrome c release and caspase activation, culminating in apoptosis. Methotrexate 0-3 mitogen-activated protein kinase 8 Homo sapiens 83-86 26083398-5 2015 The use of specific inhibitor for JNK abrogates the MTX-induced activation of pro-apoptotic proteins and downstream events confirming JNK phosphorylation by MTX as a key event. Methotrexate 52-55 mitogen-activated protein kinase 8 Homo sapiens 34-37 26083398-5 2015 The use of specific inhibitor for JNK abrogates the MTX-induced activation of pro-apoptotic proteins and downstream events confirming JNK phosphorylation by MTX as a key event. Methotrexate 52-55 mitogen-activated protein kinase 8 Homo sapiens 134-137 26083398-5 2015 The use of specific inhibitor for JNK abrogates the MTX-induced activation of pro-apoptotic proteins and downstream events confirming JNK phosphorylation by MTX as a key event. Methotrexate 157-160 mitogen-activated protein kinase 8 Homo sapiens 34-37 26083398-5 2015 The use of specific inhibitor for JNK abrogates the MTX-induced activation of pro-apoptotic proteins and downstream events confirming JNK phosphorylation by MTX as a key event. Methotrexate 157-160 mitogen-activated protein kinase 8 Homo sapiens 134-137 25912909-0 2015 The switch from ER stress-induced apoptosis to autophagy via ROS-mediated JNK/p62 signals: A survival mechanism in methotrexate-resistant choriocarcinoma cells. Methotrexate 115-127 mitogen-activated protein kinase 8 Homo sapiens 74-77 25912909-6 2015 Further experiments demonstrated that this cell death switch was regulated by ROS-mediated JNK/p62 pathway and subsequently lead to the resistance of choriocarcinoma cells to methotrexate treatment. Methotrexate 175-187 mitogen-activated protein kinase 8 Homo sapiens 91-94 25912909-7 2015 CONCLUSIONS: This study provides evidence to explain a survival mechanism of the switch from ER stress-induced apoptosis to autophagy via ROS-mediated JNK/p62 signals in methotrexate-resistant choriocarcinoma cells and may implicate the chemotherapy of methotrexate resistance in choriocarcinoma. Methotrexate 170-182 mitogen-activated protein kinase 8 Homo sapiens 151-154 25912909-7 2015 CONCLUSIONS: This study provides evidence to explain a survival mechanism of the switch from ER stress-induced apoptosis to autophagy via ROS-mediated JNK/p62 signals in methotrexate-resistant choriocarcinoma cells and may implicate the chemotherapy of methotrexate resistance in choriocarcinoma. Methotrexate 253-265 mitogen-activated protein kinase 8 Homo sapiens 151-154 22183962-0 2012 Methotrexate increases expression of cell cycle checkpoint genes via JNK activation. Methotrexate 0-12 mitogen-activated protein kinase 8 Homo sapiens 69-72 23406595-10 2013 Expression of the phosphorylated forms of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) was significantly higher in MTX-treated NPs than in nontreated NPs. Methotrexate 148-151 mitogen-activated protein kinase 8 Homo sapiens 90-113 23406595-10 2013 Expression of the phosphorylated forms of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) was significantly higher in MTX-treated NPs than in nontreated NPs. Methotrexate 148-151 mitogen-activated protein kinase 8 Homo sapiens 115-118 23406595-12 2013 CONCLUSION: MTX induces apoptosis in NPs via caspase cascades and both mitochondria-mediated and p38 MAPK/JNK pathways. Methotrexate 12-15 mitogen-activated protein kinase 8 Homo sapiens 106-109 24444433-10 2014 When U937 cells were cultured with MTX, upregulated expression of JUN and FOS, but not JNK 1 or 2, also was observed. Methotrexate 35-38 mitogen-activated protein kinase 8 Homo sapiens 87-92 22183962-7 2012 In tissue culture, MTX induced expression of both p53 and p21 by JNK-2- and JNK-1-dependent mechanisms, respectively, while CHEK2 and RANGAP1 were not induced by MTX. Methotrexate 19-22 mitogen-activated protein kinase 8 Homo sapiens 76-81 22183962-8 2012 MTX also induced ROS production, JNK activation, and sensitivity to apoptosis in activated T cells. Methotrexate 0-3 mitogen-activated protein kinase 8 Homo sapiens 33-36 22183962-10 2012 CONCLUSION: Our findings support the notion that MTX restores some, but not all, of the proteins contributing to cell cycle checkpoint deficiencies in RA T cells, via a JNK-dependent pathway. Methotrexate 49-52 mitogen-activated protein kinase 8 Homo sapiens 169-172 21618198-0 2011 Increased sensitivity to apoptosis induced by methotrexate is mediated by JNK. Methotrexate 46-58 mitogen-activated protein kinase 8 Homo sapiens 74-77 22197938-0 2012 Methotrexate modulates tight junctions through NF-kappaB, MEK, and JNK pathways. Methotrexate 0-12 mitogen-activated protein kinase 8 Homo sapiens 67-70 21618198-5 2011 RESULTS: MTX did not directly induce apoptosis but rather "primed" cells for markedly increased sensitivity to apoptosis via either mitochondrial or death receptor pathways, by a JNK-dependent mechanism. Methotrexate 9-12 mitogen-activated protein kinase 8 Homo sapiens 179-182 21618198-6 2011 Increased sensitivity to apoptosis was mediated, at least in part, by MTX-dependent production of ROS, JNK activation, and JNK-dependent induction of genes whose protein products promote apoptosis. Methotrexate 70-73 mitogen-activated protein kinase 8 Homo sapiens 103-106 21618198-8 2011 Patients with RA who were receiving low-dose MTX therapy expressed elevated levels of the JNK target gene, jun. Methotrexate 45-48 mitogen-activated protein kinase 8 Homo sapiens 90-93 21618198-9 2011 CONCLUSION: Our results support a model whereby MTX inhibits reduction of dihydrobiopterin to tetrahydrobiopterin, resulting in increased production of ROS, increased JNK activity, and increased sensitivity to apoptosis. Methotrexate 48-51 mitogen-activated protein kinase 8 Homo sapiens 167-170