Pub. Date : 2009 Feb
PMID : 19200052
9 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | TNF-alpha induction by nickel compounds is specific through ERKs/AP-1-dependent pathway in human bronchial epithelial cells. | Nickel | tumor necrosis factor | Homo sapiens |
| 2 | 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 | tumor necrosis factor | Homo sapiens |
| 3 | 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 | tumor necrosis factor | Homo sapiens |
| 4 | 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 | tumor necrosis factor | Homo sapiens |
| 5 | 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 | tumor necrosis factor | Homo sapiens |
| 6 | 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 | tumor necrosis factor | Homo sapiens |
| 7 | 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 | tumor necrosis factor | Homo sapiens |
| 8 | 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 | tumor necrosis factor | Homo sapiens |
| 9 | 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 | tumor necrosis factor | Homo sapiens |