(−)-Epigallocatechin-3-gallate Enhances the Expression of an Insulin-Inducible Transcription Factor Gene via a Phosphoinositide 3-Kinase/Atypical Protein Kinase C Lambda Pathway
Autor: | Taichi Yamamoto, Soichiro Nakamura, Ayumi Haneishi, Tamio Noguchi, Takashi Tanaka, Kazuya Yamada, Katsuhiro Takagi, Kosuke Asano |
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Rok vydání: | 2011 |
Předmět: |
Gene Expression
Biology complex mixtures Catechin Phosphatidylinositol 3-Kinases Western blot Cell Line Tumor Gene expression Basic Helix-Loop-Helix Transcription Factors medicine Animals Insulin heterocyclic compounds RNA Messenger Enzyme Inhibitors Enhancer Protein Kinase C Protein kinase C Phosphoinositide-3 Kinase Inhibitors Phosphoinositide 3-kinase medicine.diagnostic_test Liver Neoplasms food and beverages General Chemistry Molecular biology Rats Isoenzymes Cell culture biology.protein Phosphorylation sense organs Signal transduction General Agricultural and Biological Sciences Signal Transduction |
Zdroj: | Journal of Agricultural and Food Chemistry. 59:13360-13364 |
ISSN: | 1520-5118 0021-8561 |
DOI: | 10.1021/jf204016k |
Popis: | The rat enhancer of split- and hairy-related protein-1 (SHARP-1) is an insulin-inducible transcriptional repressor. In this study, we examined issues of whether (-)-epigallocatechin-3-gallate (EGCG), a green tea polyphenol, regulates the expression of the rat SHARP-1 gene and which signaling pathway mediates the regulation. When H4IIE cells were treated with EGCG, SHARP-1 mRNA levels rapidly increased. Pretreatments with inhibitors for either phosphoinositide 3-kinase (PI 3-K) or protein kinase C partially blocked EGCG induction. Atypical protein kinase C lambda (aPKCλ) is known as a downstream target of PI 3-K in the liver. When a dominant-negative form of aPKCλ was expressed, the EGCG-induced SHARP-1 mRNAs was inhibited. Finally, Western blot analysis revealed that EGCG rapidly and temporarily stimulates aPKCλ phosphorylation. Thus, we conclude that EGCG induces SHARP-1 gene expression via a PI 3-K/aPKCλ signaling pathway. |
Databáze: | OpenAIRE |
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