PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18421578-0 2008 Death receptor-4 (DR4) expression is regulated by transcription factor NF-kappaB in response to etoposide treatment. Etoposide 96-105 TNF receptor superfamily member 10a Homo sapiens 0-16 18421578-12 2008 Expression of the kinase inactive MEKK1 (MEKK1-KM) abrogates the up-regulation of DR4 after etoposide treatment. Etoposide 92-101 TNF receptor superfamily member 10a Homo sapiens 82-85 18421578-13 2008 Taken together, NF-kappaB plays a role in up-regulation of DR4 following etoposide treatment. Etoposide 73-82 TNF receptor superfamily member 10a Homo sapiens 59-62 18421578-0 2008 Death receptor-4 (DR4) expression is regulated by transcription factor NF-kappaB in response to etoposide treatment. Etoposide 96-105 TNF receptor superfamily member 10a Homo sapiens 18-21 18421578-2 2008 DNA damaging agents (genotoxins) such as etoposide increase DR4 expression and when combined with TRAIL induce a synergistic apoptotic response. Etoposide 41-50 TNF receptor superfamily member 10a Homo sapiens 60-63 18421578-5 2008 Increased expression of DR4 following etoposide treatment is blocked by inhibition of the NF-kappaB pathway. Etoposide 38-47 TNF receptor superfamily member 10a Homo sapiens 24-27 18421578-7 2008 Indeed, knockdown of p65 by RNA interference blocked etoposide up-regulation of DR4. Etoposide 53-62 TNF receptor superfamily member 10a Homo sapiens 80-83 11090076-6 2000 Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels. Etoposide 39-48 TNF receptor superfamily member 10a Homo sapiens 94-97 15634660-0 2004 Camptothecin- and etoposide-induced apoptosis in human leukemia cells is independent of cell death receptor-3 and -4 aggregation but accelerates tumor necrosis factor-related apoptosis-inducing ligand-mediated cell death. Etoposide 18-27 TNF receptor superfamily member 10a Homo sapiens 93-116 15634660-1 2004 During camptothecin- and etoposide (VP-16)-induced apoptosis in HL-60 cells, the expression level of cell death receptor-3 (DR3), cell death receptor-4 (DR4), and FAS remained mostly unchanged, whereas the expression of silencers of death domain (SODD) and FLICE inhibitory proteins, inhibitors of the cell death receptor signaling pathways, decreased substantially. Etoposide 25-34 TNF receptor superfamily member 10a Homo sapiens 135-151 14500373-4 2003 The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells. Etoposide 66-75 TNF receptor superfamily member 10a Homo sapiens 137-153 14500373-4 2003 The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells. Etoposide 66-75 TNF receptor superfamily member 10a Homo sapiens 154-157 12823542-7 2003 The RT-PCR and Western blotting results demonstrated that the levels of both mRNA and protein for death receptor-4, death receptor-5 and decoy receptor-2 remained unchanged in response to etoposide, indicating that the synergistic effect of TRAIL and etoposide is not a result of increasing the expression for TRAIL receptors, but rather is associated with amplification of the mitochondrial signal pathway. Etoposide 188-197 TNF receptor superfamily member 10a Homo sapiens 98-153 12014636-4 2002 RESULTS: Treatment with suboptimal concentrations of etoposide or doxorubicin rendered T-47D cells sensitive to anti-Fas antibody or TRAIL, consistent with Fas and TRAIL-R1 mRNA expression by T-47D cells following drug treatment. Etoposide 53-62 TNF receptor superfamily member 10a Homo sapiens 164-172 12838325-7 2003 Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5. Etoposide 102-111 TNF receptor superfamily member 10a Homo sapiens 241-244 10594023-0 2000 Increased expression of death receptors 4 and 5 synergizes the apoptosis response to combined treatment with etoposide and TRAIL. Etoposide 109-118 TNF receptor superfamily member 10a Homo sapiens 24-47 10594023-4 2000 The mechanism of the synergistic effect results from the etoposide-mediated increase in the expression of the death receptors 4 (DR4) and 5 (DR5). Etoposide 57-66 TNF receptor superfamily member 10a Homo sapiens 110-127 10594023-4 2000 The mechanism of the synergistic effect results from the etoposide-mediated increase in the expression of the death receptors 4 (DR4) and 5 (DR5). Etoposide 57-66 TNF receptor superfamily member 10a Homo sapiens 129-132 10594023-5 2000 Inhibition of NF-kappaB activation by expression of kinase-inactive MEK kinase 1(MEKK1) or dominant-negative IkappaB (DeltaIkappaB) blocked the increase in DR4 and DR5 expression following etoposide treatment. Etoposide 189-198 TNF receptor superfamily member 10a Homo sapiens 156-159 10594023-6 2000 Addition of a soluble decoy DR4 fusion protein (DR4:Fc) to cell cultures reduced the amount of etoposide-induced apoptosis in a dose-dependent manner. Etoposide 95-104 TNF receptor superfamily member 10a Homo sapiens 28-31 10594023-6 2000 Addition of a soluble decoy DR4 fusion protein (DR4:Fc) to cell cultures reduced the amount of etoposide-induced apoptosis in a dose-dependent manner. Etoposide 95-104 TNF receptor superfamily member 10a Homo sapiens 48-51 10594023-7 2000 The addition of a soluble TNF decoy receptor (TNFR:Fc) was without effect, demonstrating the specificity of DR4 binding ligands in the etoposide-induced apoptosis response. Etoposide 135-144 TNF receptor superfamily member 10a Homo sapiens 108-111