Title : Molecular mechanisms of c-Jun N-terminal kinase-mediated apoptosis induced by anticarcinogenic isothiocyanates.

Pub. Date : 1998 Jan 16

PMID : 9430725






19 Functional Relationships(s)
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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