Abstract
To determine whether c-fos/c-jun (AP-1) and CREB mediate glucocorticoid stimulated TRH gene regulation, we investigated the effect of N-ethyl-maleimide (NEM), an alkylating agent, and 12-O-tetradecanoylphorbol-13-acetate (TPA) on this process. NEM decreased while TPA increased TRH levels in rat hypothalamic culture, changes similar to their effects on CREB and Fos/Jun proteins in the AtT20 cell line. This suggests that glucocorticoid stimulation of TRH gene expression may be regulated by the AP-1 complex and CREB pathway.
MeSH terms
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Animals
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Cells, Cultured
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Cyclic AMP Response Element-Binding Protein / metabolism*
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Dexamethasone / pharmacology*
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Dimerization
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Ethylmaleimide / pharmacology*
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Fetus
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / physiology*
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Genes, fos
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Genes, jun
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Hypothalamus / cytology
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Hypothalamus / metabolism*
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Neurons / cytology
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Neurons / drug effects
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Neurons / metabolism*
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Rats
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Tetradecanoylphorbol Acetate / pharmacology*
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Thyrotropin-Releasing Hormone / genetics*
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Transcription Factor AP-1 / metabolism*
Substances
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Cyclic AMP Response Element-Binding Protein
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Transcription Factor AP-1
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Thyrotropin-Releasing Hormone
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Dexamethasone
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Tetradecanoylphorbol Acetate
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Ethylmaleimide