PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9020192-2 1997 In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells. Etoposide 36-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-91 10913345-0 2000 Activation of the tumor metastasis suppressor gene, KAI1, by etoposide is mediated by p53 and c-Jun genes. Etoposide 61-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-99 10454518-3 1999 Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with phosphorylation and activation of the c-Jun NH(2)-terminal kinase (JNK1) SAPK enzymes p46 and p54-JNK2 and transient increases in expression of the transcription factor c-Jun, a primary JNK substrate. Etoposide 81-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 162-167 10811113-2 2000 The induction of the CD95/CD95L pathway can be activated by the activator protein-1 (AP-1)-mediated up-regulation of the CD95L promoter, which is responsible for the induction of apoptosis elicited by stimuli such as etoposide. Etoposide 217-226 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-83 10811113-2 2000 The induction of the CD95/CD95L pathway can be activated by the activator protein-1 (AP-1)-mediated up-regulation of the CD95L promoter, which is responsible for the induction of apoptosis elicited by stimuli such as etoposide. Etoposide 217-226 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 85-89 10454518-3 1999 Induction of apoptotic cell death and DNA damage by treatment of U937 cells with etoposide (100 microM) was associated with phosphorylation and activation of the c-Jun NH(2)-terminal kinase (JNK1) SAPK enzymes p46 and p54-JNK2 and transient increases in expression of the transcription factor c-Jun, a primary JNK substrate. Etoposide 81-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 293-298 9020192-2 1997 In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells. Etoposide 36-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-172 9816016-1 1995 Previous reports have demonstrated that a variety of anticancer drugs, e.g., 1-beta-D-arabinofuranosylcytosine (ara-C), mitoxantrone, etoposide, camptothecin, and cisplatin, induce the expression of c-jun oncogene in leukemic cells prior to producing internucleosomal DNA fragmentation and the morphological features of apoptosis. Etoposide 134-143 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 199-204 1904980-9 1991 These findings suggest that transcriptional induction of c-jun expression represents a signaling pathway activated in the cellular response to etoposide-induced DNA damage. Etoposide 143-152 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 8068039-0 1994 Increased c-jun/AP-1 levels in etoposide-resistant human leukemia K562 cells. Etoposide 31-40 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 10-15 8068039-0 1994 Increased c-jun/AP-1 levels in etoposide-resistant human leukemia K562 cells. Etoposide 31-40 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-20 8267650-7 1993 Basal levels of c-myc were comparable for all three cell lines, but levels of c-jun and c-fos were elevated 2- to 4-fold in VP-16-resistant cell lines. Etoposide 124-129 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-83 8267650-9 1993 Exposure of both sensitive and resistant cells to 200 microM VP-16 for 5 hr resulted in no further changes in topoisomerase II mRNA levels but caused an additional 2- to 3-fold elevation in the level of c-jun mRNA, indicating that altered basal levels of this gene were not due to deregulation of this gene. Etoposide 61-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 203-208 1904980-0 1991 Activation of the c-jun protooncogene in human myeloid leukemia cells treated with etoposide. Etoposide 83-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-23 1904980-3 1991 The present results demonstrate that etoposide induces expression of the c-jun protooncogene in HL-60 myeloid leukemia cells. Etoposide 37-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 1904980-6 1991 Nuclear run-on assays demonstrated that the induction of c-jun expression by etoposide is regulated at the transcriptional level. Etoposide 77-86 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 1904980-7 1991 The results further demonstrate that etoposide-induced c-jun expression occurs in association with the appearance of c-fos transcripts. Etoposide 37-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 55-60 1904980-8 1991 Moreover, the c-jun gene is induced by etoposide during periods of oligonucleosomal DNA cleavage, which is characteristic of programmed cell death. Etoposide 39-48 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-19 26858249-0 2016 Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner. Etoposide 58-67 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 26858249-5 2016 Ablation of c-Jun/c-Fos or ID1 expression enhanced etoposide-mediated apoptosis through increasing activity of caspase 3 and PARP cleavage. Etoposide 51-60 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 12-17 19794957-0 2009 Hypoxia-induced decrease in p53 protein level and increase in c-jun DNA binding activity results in cancer cell resistance to etoposide. Etoposide 126-135 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-67 21610153-0 2011 Inhibiting the mTOR pathway synergistically enhances cytotoxicity in ovarian cancer cells induced by etoposide through upregulation of c-Jun. Etoposide 101-110 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-140 21610153-11 2011 The synergistic interaction of rapamycin and etoposide was lower when the c-Jun pathway was suppressed by a c-Jun N-terminal kinase inhibitor (SP600125). Etoposide 45-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 21610153-11 2011 The synergistic interaction of rapamycin and etoposide was lower when the c-Jun pathway was suppressed by a c-Jun N-terminal kinase inhibitor (SP600125). Etoposide 45-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 108-113 19794957-9 2009 Conversely, hypoxia increased c-jun DNA binding activity in the presence of etoposide. Etoposide 76-85 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 19794957-10 2009 siRNA-mediated silencing of c-jun increased the responsiveness of cells to etoposide under hypoxia, as shown by an increase in caspase 3 activity and lactate dehydrogenase release. Etoposide 75-84 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 19794957-12 2009 These data evidenced that hypoxia decreased the responsiveness of HepG2 cells to etoposide at least by two independent pathways involving p53 inhibition and c-jun activation. Etoposide 81-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-162 17920329-4 2008 Here, we show that following a short exposure to the DNA-damaging compound etoposide, c-Jun phosphorylation is restricted to S63/S73. Etoposide 75-84 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-91