PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7720792-0 1995 Tunicamycin potently inhibits tumor necrosis factor-induced hepatocyte apoptosis. Tunicamycin 0-11 tumor necrosis factor Mus musculus 30-51 16107336-6 2005 Conversely, the UPR induced by tunicamycin substantially suppresses TNFalpha-induced ROS accumulation and cell death by inhibiting reduction of cellular glutathione levels. Tunicamycin 31-42 tumor necrosis factor Mus musculus 68-76 10973810-2 2000 When J774.1 cells were pretreated with tunicamycin, their granulocytin-dependent TNF-alpha production was greatly reduced. Tunicamycin 39-50 tumor necrosis factor Mus musculus 81-90 9237560-9 1997 There were a number of precursor TNF isoforms that were unchanged upon tunicamycin treatment and these presumably reflect protein modifications other than glycosylation. Tunicamycin 71-82 tumor necrosis factor Mus musculus 33-36 7720792-1 1995 The protein glycosylation inhibitor tunicamycin protected male BALB/c mice from tumor necrosis factor alpha-induced liver failure. Tunicamycin 36-47 tumor necrosis factor Mus musculus 80-101 7720792-2 1995 Tunicamycin also inhibited tumor necrosis factor-induced cell death in primary hepatocyte cultures with a median inhibitory concentration of 8 nM, but not in the tumor cell line WEHI 164 clone 13. Tunicamycin 0-11 tumor necrosis factor Mus musculus 27-48 30034372-8 2018 Tunicamycin-treated bacteria or the bacterial WTA preparation suppressed NF-kappaB and inflammatory cytokine production (TNFalpha, and IL-6) from murine macrophage cell line (RAW 264.7) indicating the reduced WTA level possibly attenuates an inflammatory response. Tunicamycin 0-11 tumor necrosis factor Mus musculus 121-129 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 tumor necrosis factor Mus musculus 167-176 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 tumor necrosis factor Mus musculus 264-273 32057287-11 2020 Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-alpha expression in lung tissues and BALF. Tunicamycin 33-35 tumor necrosis factor Mus musculus 197-206 25630719-10 2015 In vitro, ER stress induced by tunicamycin synergistically increased LPS-triggered pro-inflammatory cytokine induction and promoted the activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathway in bone marrow-derived macrophages; moreover, tunicamycin also cooperated with TNF-alpha to increase hepatocyte apoptosis. Tunicamycin 31-42 tumor necrosis factor Mus musculus 315-324 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 tumor necrosis factor Mus musculus 68-72 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 tumor necrosis factor Mus musculus 101-105 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 tumor necrosis factor Mus musculus 166-175 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 tumor necrosis factor Mus musculus 183-210 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 tumor necrosis factor Mus musculus 212-221 21150875-2 2011 Since tumor necrosis factor alpha (TNFalpha) plays a role in acute kidney injury, and induces ER stress and cell death in vitro, we examined the contribution of TNFalpha to acute kidney ER stress induced by tunicamycin. Tunicamycin 207-218 tumor necrosis factor Mus musculus 161-169 21150875-3 2011 Contrary to expectation, tunicamycin caused much more severe kidney injury in TNFalpha-/- than in wild-type mice. Tunicamycin 25-36 tumor necrosis factor Mus musculus 78-86 21150875-5 2011 Reconstitution of TNFalpha-/- mice with TNFalpha 24 h before tunicamycin injection reversed the susceptibility. Tunicamycin 61-72 tumor necrosis factor Mus musculus 18-26 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor Mus musculus 5-13 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor Mus musculus 160-168 18799549-6 2008 In tumor necrosis factor (TNF)-alpha-treated cells, suppression of MCP-1 by indomethacin was inversely correlated with induction of UPR, and other inducers of UPR including tunicamycin, thapsigargin, and A23187 reproduced the suppressive effect. Tunicamycin 173-184 tumor necrosis factor Mus musculus 3-36