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   <subfield code="a">Activation of Signal Transduction Kinases by Tamoxifen</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Jauh-Lin Duh, Rong Yu, Jie-Jun Jiao, George Matwyshyn, Wei Li, Tse-Hua Tan, A.-N. Kong]</subfield>
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   <subfield code="a">Purpose. To study the signal transduction mechanisms of tamoxifen via the activation of MAPKs, JNK and ERK in order to understand its regulation of gene expression. Methods. The effects of tamoxifen (TAM) on the activation of serine/ threonine mitogen-activated protein kinase (MAPK, p42/ERK2) and the stress-activated protein kinases (p46 SAPK or c-Jun N-terminal kinase, JNK1) were evaluated using a human cervical epitheloid carcinoma HeLa cell line. Results. TAM activated both JNK1 and ERK2 activities in a time- and dose-dependent manner in HeLa cells. The activation of JNK1 was enhanced when the cells were pretreated with prooxidant H2O2. Conclusions. These studies show that TAM activates the signal transduction kinases, JNK1 and ERK2, which may play important roles in the regulation of gene expression by TAM.</subfield>
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