PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27383320-0 2016 Role of TNF-alpha polymorphism in patients with nickel allergy: a marker of susceptibility to contact polysensitization. Nickel 48-54 tumor necrosis factor Homo sapiens 8-17 27467530-3 2016 In the current studies, we identified SQSTM1/p62 as a novel nickel-upregulated protein that is important for nickel-induced inflammatory TNF expression, subsequently resulting in transformation of human bronchial epithelial cells. Nickel 60-66 tumor necrosis factor Homo sapiens 137-140 27467530-3 2016 In the current studies, we identified SQSTM1/p62 as a novel nickel-upregulated protein that is important for nickel-induced inflammatory TNF expression, subsequently resulting in transformation of human bronchial epithelial cells. Nickel 109-115 tumor necrosis factor Homo sapiens 137-140 27467530-9 2016 Furthermore, SQSTM1 upregulation exhibited its promotion of nickel-induced cell transformation through exerting an impetus for nickel-induced inflammatory TNF mRNA stability. Nickel 60-66 tumor necrosis factor Homo sapiens 155-158 27467530-9 2016 Furthermore, SQSTM1 upregulation exhibited its promotion of nickel-induced cell transformation through exerting an impetus for nickel-induced inflammatory TNF mRNA stability. Nickel 127-133 tumor necrosis factor Homo sapiens 155-158 27467530-10 2016 Consistently, the MTOR-ULK1-BECN1 autophagic cascade acted as an inhibitory effect on nickel-induced TNF expression and cell transformation. Nickel 86-92 tumor necrosis factor Homo sapiens 101-104 27383320-5 2016 PATIENTS AND METHODS: To evaluate the expression of TNF-alpha polymorphism in patients with allergic contact dermatitis and in healthy people, 41 patients with allergic contact dermatitis to nickel and 40 healthy controls were enrolled. Nickel 191-197 tumor necrosis factor Homo sapiens 52-61 27383320-10 2016 CONCLUSIONS: The carriage of the TNFA-308 A/A and GA genotype may act as a marker of enhanced susceptibility to contact polysensitization, indicating that TNF-alpha is a key regulator of the initiation of delayed-type hypersensitivity reactions, the polymorphism seems to be not enough for the development of nickel monosensitization. Nickel 309-315 tumor necrosis factor Homo sapiens 33-37 27383320-10 2016 CONCLUSIONS: The carriage of the TNFA-308 A/A and GA genotype may act as a marker of enhanced susceptibility to contact polysensitization, indicating that TNF-alpha is a key regulator of the initiation of delayed-type hypersensitivity reactions, the polymorphism seems to be not enough for the development of nickel monosensitization. Nickel 309-315 tumor necrosis factor Homo sapiens 155-164 23056446-7 2012 If nickel was used as a stimulus, blockage of PD-L1 led to high amounts of TNF-alpha and IL-22. Nickel 3-9 tumor necrosis factor Homo sapiens 75-84 19200052-0 2009 TNF-alpha induction by nickel compounds is specific through ERKs/AP-1-dependent pathway in human bronchial epithelial cells. Nickel 23-29 tumor necrosis factor Homo sapiens 0-9 19200052-3 2009 The current study demonstrates that exposure of human bronchial epithelial cells (Beas-2B) to nickel compounds results in the induction of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and transactivation of nuclear factor of activated T cells (NFAT), nuclear factor-kappaB (NF-kappaB), and activator protein-1 (AP-1). Nickel 94-100 tumor necrosis factor Homo sapiens 165-192 19200052-3 2009 The current study demonstrates that exposure of human bronchial epithelial cells (Beas-2B) to nickel compounds results in the induction of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and transactivation of nuclear factor of activated T cells (NFAT), nuclear factor-kappaB (NF-kappaB), and activator protein-1 (AP-1). Nickel 94-100 tumor necrosis factor Homo sapiens 194-203 19200052-4 2009 Further studies show that neither overexpression of IKKbeta-KM, a kinase inactive mutant of IKKbeta, nor the ectopic expression of a dominant negative mutant of NFAT could inhibit the TNF-alpha induction by nickel exposure. Nickel 207-213 tumor necrosis factor Homo sapiens 184-193 19200052-5 2009 Overexpression of TAM67, a dominant-negative mutant of c-Jun, dramatically reduced the TNF-alpha induction, suggesting that AP-1 is a mediator of TNF-alpha induction in nickel responses. Nickel 169-175 tumor necrosis factor Homo sapiens 87-96 19200052-5 2009 Overexpression of TAM67, a dominant-negative mutant of c-Jun, dramatically reduced the TNF-alpha induction, suggesting that AP-1 is a mediator of TNF-alpha induction in nickel responses. Nickel 169-175 tumor necrosis factor Homo sapiens 146-155 19200052-6 2009 Our results show that ERKs are AP-1 upstream kinases responsible for TNF-alpha induction by nickel exposure; although JNKs, ERKs, and p38K were all activated in the Beas-2B cells exposed to nickel compounds. Nickel 92-98 tumor necrosis factor Homo sapiens 69-78 19200052-6 2009 Our results show that ERKs are AP-1 upstream kinases responsible for TNF-alpha induction by nickel exposure; although JNKs, ERKs, and p38K were all activated in the Beas-2B cells exposed to nickel compounds. Nickel 190-196 tumor necrosis factor Homo sapiens 69-78 19200052-7 2009 Our results demonstrate that inflammatory TNF-alpha could be induced by nickel exposure in Beas-2B cells specifically through an ERKs/AP-1-dependent pathway. Nickel 72-78 tumor necrosis factor Homo sapiens 42-51 31682627-4 2019 Hypoxia-mimicking conditions, which include NiCl2, CoCl2, and DMOG, an inhibitor of 2-oxoglutarate-dependent enzymes, also selectively inhibited TNF-alpha-induced TSLP expression. Nickel 44-49 tumor necrosis factor Homo sapiens 145-154 12930308-5 2003 Western blot analysis demonstrated that nickel ions induced up-modulation of the expression of the keratinocyte growth factor receptors (KGFR) without affecting the keratinocyte differentiation, whereas the protein levels of the epidermal growth factor receptor (EGFR) and of its ligand transforming growth factor-alpha (TGF-alpha) appeared unmodified by the treatment. Nickel 40-46 tumor necrosis factor Homo sapiens 287-319 11919079-0 2002 Dose-related protection from nickel-induced lung injury in transgenic mice expressing human transforming growth factor-alpha. Nickel 29-35 tumor necrosis factor Homo sapiens 92-124 9886425-3 1999 Skin affected with ACD to nickel and skin-derived, nickel-specific CD4+ T cell lines expressed IFN-gamma, TNF-alpha, and IL-17 mRNAs. Nickel 51-57 tumor necrosis factor Homo sapiens 106-115 9886425-4 1999 Four of seven nickel-specific CD4+ T cell clones positive for the skin-homing receptor, cutaneous lymphocyte-associated Ag, were shown to corelease IL-17, IFN-gamma, and TNF-alpha. Nickel 14-20 tumor necrosis factor Homo sapiens 170-179 31943712-5 2020 The results showed that nickel could induce cell apoptosis, increase oxidative stress, and promote the expression of pro-inflammatory cytokines, including tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, IL-8, C-reaction protein. Nickel 24-30 tumor necrosis factor Homo sapiens 155-182 31822637-3 2019 Here, we demonstrated that NiCl2 activated nuclear factor kappa B (NF-kappaB), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1beta (IL-1beta), -6, -8, -18, tumor necrosis factor-alpha (TNF-alpha) and interferon beta (INF-beta). Nickel 27-32 tumor necrosis factor Homo sapiens 324-351 31822637-3 2019 Here, we demonstrated that NiCl2 activated nuclear factor kappa B (NF-kappaB), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1beta (IL-1beta), -6, -8, -18, tumor necrosis factor-alpha (TNF-alpha) and interferon beta (INF-beta). Nickel 27-32 tumor necrosis factor Homo sapiens 353-362 15304089-0 2004 Nickel and DNCB induce CCR7 expression on human dendritic cells through different signalling pathways: role of TNF-alpha and MAPK. Nickel 0-6 tumor necrosis factor Homo sapiens 111-120 7864660-3 1994 Our aim was to assess the effects of sensitizing metal haptens (nickel, cobalt and chromium) compared with the toxic metal cadmium on the induction of ICAM-1 and the production of TNF alpha by epidermal cells. Nickel 64-70 tumor necrosis factor Homo sapiens 180-189