PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18977528-8 2009 The inhibition of NF-kappaB with BAY 11-7082 increased the cytotoxicity of imatinib in K562-Vinc cells but not in K562-WT. Imatinib Mesylate 75-83 nuclear factor kappa B subunit 1 Homo sapiens 18-27 19378338-0 2009 NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants. Imatinib Mesylate 39-47 nuclear factor kappa B subunit 1 Homo sapiens 0-9 19378338-0 2009 NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants. Imatinib Mesylate 62-70 nuclear factor kappa B subunit 1 Homo sapiens 0-9 19378338-8 2009 Our data strongly support the targeting of NF-kappaB as a promising new therapeutic opportunity for the treatment of imatinib resistant CML patients in particular in the case of T315I patients. Imatinib Mesylate 117-125 nuclear factor kappa B subunit 1 Homo sapiens 43-52 16174751-6 2005 In line with this observation, phosphorylation of IkappaB and subsequent DNA binding of NF-kappaB, which is critically involved in TNF-alpha, but not IL-10 expression, was reduced by imatinib. Imatinib Mesylate 183-191 nuclear factor kappa B subunit 1 Homo sapiens 88-97 18245668-5 2008 Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL. Imatinib Mesylate 190-198 nuclear factor kappa B subunit 1 Homo sapiens 103-112 18619726-4 2008 Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib. Imatinib Mesylate 170-178 nuclear factor kappa B subunit 1 Homo sapiens 73-95 18619726-4 2008 Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib. Imatinib Mesylate 170-178 nuclear factor kappa B subunit 1 Homo sapiens 97-106 18245668-5 2008 Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL. Imatinib Mesylate 223-231 nuclear factor kappa B subunit 1 Homo sapiens 103-112 18245668-7 2008 These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia. Imatinib Mesylate 162-170 nuclear factor kappa B subunit 1 Homo sapiens 53-62 10979973-7 2000 CGP57148B also inhibited constitutively active Akt kinase and NFkappaB in Bcr-Abl-positive cells. Imatinib Mesylate 0-9 nuclear factor kappa B subunit 1 Homo sapiens 62-70 33289342-0 2021 Sulfasalazine synergistically enhances the inhibitory effects of imatinib against hepatocellular carcinoma (HCC) cells by targeting NFkappaB, BCR/ABL, and PI3K/AKT signaling pathway-related proteins. Imatinib Mesylate 65-73 nuclear factor kappa B subunit 1 Homo sapiens 132-140 29945498-2 2018 Constitutive activation of NFkappaB and beta-catenin signaling promotes cellular proliferation and survival and resistance to Imatinib therapy in CML. Imatinib Mesylate 126-134 nuclear factor kappa B subunit 1 Homo sapiens 27-35 33527482-8 2021 Mechanistically, imatinib or BCR-ABL siRNA following deglutathionylation of NF-kappaB, enhanced its binding to iNOS promoter and induced iNOS transcription. Imatinib Mesylate 17-25 nuclear factor kappa B subunit 1 Homo sapiens 76-85 29945498-6 2018 RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins. Imatinib Mesylate 89-97 nuclear factor kappa B subunit 1 Homo sapiens 26-34 29945498-10 2018 Targeting Akirin-2, NFkappaB and beta-catenin genes may provide an opportunity to overcome imatinib resistance in CML. Imatinib Mesylate 91-99 nuclear factor kappa B subunit 1 Homo sapiens 20-28 26874514-9 2016 The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin. Imatinib Mesylate 63-71 nuclear factor kappa B subunit 1 Homo sapiens 130-151 26874514-9 2016 The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin. Imatinib Mesylate 63-71 nuclear factor kappa B subunit 1 Homo sapiens 153-162 24125838-6 2013 Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway. Imatinib Mesylate 87-95 nuclear factor kappa B subunit 1 Homo sapiens 248-257 24125838-6 2013 Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway. Imatinib Mesylate 187-195 nuclear factor kappa B subunit 1 Homo sapiens 123-132 24125838-6 2013 Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway. Imatinib Mesylate 187-195 nuclear factor kappa B subunit 1 Homo sapiens 248-257 23892407-12 2013 In DOX-resistant cells, Imatinib treatment reduced IkappaBalpha tyrosine phosphorylation and NF-kappaB activity. Imatinib Mesylate 24-32 nuclear factor kappa B subunit 1 Homo sapiens 93-102 23383209-0 2013 Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1. Imatinib Mesylate 0-8 nuclear factor kappa B subunit 1 Homo sapiens 84-93 23383209-5 2013 Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway. Imatinib Mesylate 15-23 nuclear factor kappa B subunit 1 Homo sapiens 88-97 23383209-5 2013 Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway. Imatinib Mesylate 15-23 nuclear factor kappa B subunit 1 Homo sapiens 141-150 23383209-8 2013 Furthermore, since imatinib converts a master survival regulator, NF-kappaB, from a pro-survival into a pro-apoptotic factor, our data suggest that NF-kappaB inhibitors may be ineffective in sensitizing tumors containing activated c-Abl/Arg to anthracyclines, and instead might antagonize anthracycline-induced apoptosis. Imatinib Mesylate 19-27 nuclear factor kappa B subunit 1 Homo sapiens 66-75 21935477-3 2011 The aim of this study was to investigate control of NF-kappaB post-translational modifications exerted by Imatinib and whether any such effects are associated with altered islet gene expression and chemokine production in vitro. Imatinib Mesylate 106-114 nuclear factor kappa B subunit 1 Homo sapiens 52-61 21935477-14 2011 CONCLUSION: Imatinib by itself promotes a modest activation of NF-kappaB. Imatinib Mesylate 12-20 nuclear factor kappa B subunit 1 Homo sapiens 63-72 21935477-16 2011 It is possible that Imatinib induces NF-kappaB preconditioning of islet cells leading to lowered cytokine sensitivity and a mitigated islet inflammation. Imatinib Mesylate 20-28 nuclear factor kappa B subunit 1 Homo sapiens 37-46