PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29773987-7 2018 Moreover, CSL when administered either alone or in combination with bortezomib inhibited MM tumor growth and decreased serum IL-6 and TNF-alpha levels. Bortezomib 68-78 tumor necrosis factor Mus musculus 134-143 30914235-10 2019 The bortezomib group exhibited significantly higher expression of pro-apoptotic protein TNF-alpha (p = 0.032), and lower expression of anti-apoptotic protein XIAP, Stat3, and Survivin (p = 0.024, 0.016, and 0.039, respectively). Bortezomib 4-14 tumor necrosis factor Mus musculus 88-97 24406455-0 2014 Treatment with anti-TNF alpha protects against the neuropathy induced by the proteasome inhibitor bortezomib in a mouse model. Bortezomib 98-108 tumor necrosis factor Mus musculus 20-29 28487944-10 2017 Furthermore, it was also revealed that bortezomib was able to reduce serum levels of CRP and TNF-alpha caused by DSS and increase the level of ALB in serum and the activity of SOD in colonic tissues. Bortezomib 39-49 tumor necrosis factor Mus musculus 93-102 28800777-14 2017 Following two injections of Bz, serum IL-6 and TNF-alpha levels were significantly more elevated in 14-week-old than in 10-week-old mice. Bortezomib 28-30 tumor necrosis factor Mus musculus 47-56 24530998-0 2014 TNF-alpha-mediated JNK activation in the dorsal root ganglion neurons contributes to Bortezomib-induced peripheral neuropathy. Bortezomib 85-95 tumor necrosis factor Mus musculus 0-9 24530998-4 2014 Furthermore, the TNF-alpha synthesis inhibitor thalidomide significantly blocked the activation of both isoforms JNK1 and JNK2 in the DRG and attenuated mechanical allodynia following BTZ treatment. Bortezomib 184-187 tumor necrosis factor Mus musculus 17-26 24530998-5 2014 Knockout of the expression of TNF-alpha receptor TNFR1 (TNFR1 KO mice) or TNFR2 (TNFR2 KO mice) inhibited JNK1 and JNK2 activation and decreased mechanical allodynia induced by BTZ. Bortezomib 177-180 tumor necrosis factor Mus musculus 30-39 24530998-6 2014 These results suggest that upregulated TNF-alpha expression may activate JNK signaling via TNFR1 or TNFR2 to mediate mechanical allodynia following BTZ treatment. Bortezomib 148-151 tumor necrosis factor Mus musculus 39-48 24406455-4 2014 Release of proinflammatory cytokines after nerve damage can induce neurodegeneration, but the effects of BTZ on cytokine expression in neurons are unknown, although BTZ modulates the expression of cytokines, such as TNF-alpha and IL-6, in tumor cells. Bortezomib 165-168 tumor necrosis factor Mus musculus 216-225 24406455-9 2014 We conclude that monoclonal antibodies directed against TNF-alpha may be a suitable neuroprotective therapy against the neurotoxicity induced by BTZ. Bortezomib 145-148 tumor necrosis factor Mus musculus 56-65 24022788-9 2013 Inhibition of the UPP with bortezomib significantly improved muscle function and also significantly reduced tumor necrosis factor alpha expression in the skeletal muscle of mice with myositis. Bortezomib 27-37 tumor necrosis factor Mus musculus 108-135 16397116-8 2006 Finally, the induction of UPase by TNF-alpha could be suppressed by PS-341, a NF-kappaB inhibitor. Bortezomib 68-74 tumor necrosis factor Mus musculus 35-44 21360496-12 2011 CONCLUSION: In TNF-mediated bone destruction, bortezomib treatment increased synovial osteoclastogenesis and bone destruction. Bortezomib 46-56 tumor necrosis factor Mus musculus 15-18 17373661-0 2007 TNF potentiates anticancer activity of bortezomib (Velcade) through reduced expression of proteasome subunits and dysregulation of unfolded protein response. Bortezomib 39-49 tumor necrosis factor Mus musculus 0-3 17373661-0 2007 TNF potentiates anticancer activity of bortezomib (Velcade) through reduced expression of proteasome subunits and dysregulation of unfolded protein response. Bortezomib 51-58 tumor necrosis factor Mus musculus 0-3 17373661-3 2007 In the present work we demonstrate enhanced anticancer activity of bortezomib by its combination with tumor necrosis factor (TNF) in the experimental model of C-26 colon carcinoma in mice. Bortezomib 67-77 tumor necrosis factor Mus musculus 102-123 17373661-3 2007 In the present work we demonstrate enhanced anticancer activity of bortezomib by its combination with tumor necrosis factor (TNF) in the experimental model of C-26 colon carcinoma in mice. Bortezomib 67-77 tumor necrosis factor Mus musculus 125-128 17373661-7 2007 Moreover, TNF interfered with bortezomib-induced upregulation of distinct subunits of the 26S proteasome. Bortezomib 30-40 tumor necrosis factor Mus musculus 10-13 17328981-8 2007 Bortezomib induced significant decrements of mRNA expression of TNF-alpha and IL-6. Bortezomib 0-10 tumor necrosis factor Mus musculus 64-73 16670342-5 2006 Furthermore, in that inhibitors of the Akt pathway can sensitize otherwise resistant TBJ/Neuro-2a cells to apoptosis induced by IFN-gamma plus TNF-alpha, we hypothesized that bortezomib also could sensitize these cells to IFN-gamma plus TNF-alpha. Bortezomib 175-185 tumor necrosis factor Mus musculus 237-246 16670342-6 2006 We demonstrate for the first time that bortezomib not only up-regulates the expression of receptors for IFN-gamma and TNF-alpha on both TBJ neuroblastoma and EOMA endothelial cell lines, but also markedly enhances the sensitivity of these cells to apoptosis induced by IFN-gamma plus TNF-alpha in vitro. Bortezomib 39-49 tumor necrosis factor Mus musculus 118-127 16670342-6 2006 We demonstrate for the first time that bortezomib not only up-regulates the expression of receptors for IFN-gamma and TNF-alpha on both TBJ neuroblastoma and EOMA endothelial cell lines, but also markedly enhances the sensitivity of these cells to apoptosis induced by IFN-gamma plus TNF-alpha in vitro. Bortezomib 39-49 tumor necrosis factor Mus musculus 284-293 16670342-7 2006 Furthermore, bortezomib enhances the in vivo antitumor efficacy of IFN-gamma/TNF-alpha-inducing cytokines, including both IL-2 and IL-12 in mice bearing well-established primary and/or metastatic TBJ neuroblastoma tumors. Bortezomib 13-23 tumor necrosis factor Mus musculus 77-86 16585569-6 2006 In vitro lytic assays demonstrated that TNF-alpha, but not perforin, Fas-ligand, or TRAIL, was responsible for bortezomib-sensitized B16 cytotoxicity. Bortezomib 111-121 tumor necrosis factor Mus musculus 40-49 22427154-6 2012 Bzb treatment significantly reduced the expression of TNF-alpha, IL-1beta, IL-6, MCP-1, MIP-1alpha, iNOS, and COX-2 and induced the expression of IL-10 in a time-dependent manner. Bortezomib 0-3 tumor necrosis factor Mus musculus 54-63 18539902-9 2008 These results indicate that decreased toxicity and increased efficacy of bortezomib in murine allo-BMT can be achieved by removal of CD4(+) T cells from the graft or by inhibiting TNFalpha. Bortezomib 73-83 tumor necrosis factor Mus musculus 180-188 17373661-6 2007 TNF prevented the upregulation of Hsp27 induced by bortezomib, which may contribute to enhanced ER stress. Bortezomib 51-61 tumor necrosis factor Mus musculus 0-3 32221318-5 2020 We found that Al particles and BTZ attenuated the expression of inflammatory cytokines (IL-1beta, IL-6, TNF-alpha). Bortezomib 31-34 tumor necrosis factor Mus musculus 104-113