Pub. Date : 1998 Jan 16
PMID : 9430725
19 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Molecular mechanisms of c-Jun N-terminal kinase-mediated apoptosis induced by anticarcinogenic isothiocyanates. | Isothiocyanates | mitogen-activated protein kinase 8 | Homo sapiens |
| 2 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenylmethyl isocyacyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 3 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenylmethyl isocyacyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 4 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | pmitc | mitogen-activated protein kinase 8 | Homo sapiens |
| 5 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | pmitc | mitogen-activated protein kinase 8 | Homo sapiens |
| 6 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 7 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 8 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 9 | Here, we report that phenylmethyl isocyacyanate (PMITC) and phenylethyl isothiocyanate (PEITC) induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 10 | The sustained JNK activation caused by isothiocyanates was associated with apoptosis induction in various cell types. | Isothiocyanates | mitogen-activated protein kinase 8 | Homo sapiens |
| 11 | An inhibitor of the caspase/interleukin-1 beta-converting enzyme blocked isothiocyanate-induced apoptosis without inhibiting the JNK activation, which suggests that JNK activation by isothiocyanates is an event that is independent or upstream of the activation of caspase/interleukin-1 beta-converting enzyme proteases. | isothiocyanic acid | mitogen-activated protein kinase 8 | Homo sapiens |
| 12 | An inhibitor of the caspase/interleukin-1 beta-converting enzyme blocked isothiocyanate-induced apoptosis without inhibiting the JNK activation, which suggests that JNK activation by isothiocyanates is an event that is independent or upstream of the activation of caspase/interleukin-1 beta-converting enzyme proteases. | Isothiocyanates | mitogen-activated protein kinase 8 | Homo sapiens |
| 13 | PEITC-induced apoptosis was suppressed by interfering with the JNK pathway with a dominant-negative mutant of JNK1 or MEKK1 (JNK1(APF) and MEKK1 (KR), respectively), implying that the JNK pathway is required for apoptotic signaling. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 14 | PEITC-induced apoptosis was suppressed by interfering with the JNK pathway with a dominant-negative mutant of JNK1 or MEKK1 (JNK1(APF) and MEKK1 (KR), respectively), implying that the JNK pathway is required for apoptotic signaling. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 15 | PEITC-induced apoptosis was suppressed by interfering with the JNK pathway with a dominant-negative mutant of JNK1 or MEKK1 (JNK1(APF) and MEKK1 (KR), respectively), implying that the JNK pathway is required for apoptotic signaling. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 16 | PEITC-induced apoptosis was suppressed by interfering with the JNK pathway with a dominant-negative mutant of JNK1 or MEKK1 (JNK1(APF) and MEKK1 (KR), respectively), implying that the JNK pathway is required for apoptotic signaling. | phenethyl isothiocyanate | mitogen-activated protein kinase 8 | Homo sapiens |
| 17 | Isothiocyanate-induced JNK activation was blocked by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling was triggered by oxidative stress. | isothiocyanic acid | mitogen-activated protein kinase 8 | Homo sapiens |
| 18 | Isothiocyanate-induced JNK activation was blocked by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling was triggered by oxidative stress. | Mercaptoethanol | mitogen-activated protein kinase 8 | Homo sapiens |
| 19 | Isothiocyanate-induced JNK activation was blocked by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling was triggered by oxidative stress. | Acetylcysteine | mitogen-activated protein kinase 8 | Homo sapiens |