Abstract
Phosphoenolpyruvate carboxykinase (PEPCK) governs the rate-limiting step in gluconeogenesis. Glucocorticoids and adenosine 3',5'-monophosphate (cAMP) increase PEPCK gene transcription and gluconeogenesis, whereas insulin has the opposite effect. Insulin is dominant, since it prevents cAMP and glucocorticoid-stimulated transcription. Glucocorticoid and cAMP response elements have been located in the PEPCK gene and now a 15-base pair insulin-responsive sequence (IRS) is described. Evidence for a binding activity that recognizes this sequence is presented.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Base Sequence
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Cell Line
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Chloramphenicol O-Acetyltransferase / genetics
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Chloramphenicol O-Acetyltransferase / metabolism
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Cyclic AMP / analogs & derivatives
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Cyclic AMP / physiology
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Dexamethasone / pharmacology
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Genes, Regulator*
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Insulin / pharmacology*
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Molecular Sequence Data
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Phosphoenolpyruvate Carboxykinase (GTP) / genetics*
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Phosphoenolpyruvate Carboxykinase (GTP) / metabolism
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RNA, Messenger / drug effects
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RNA, Messenger / genetics
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Recombinant Fusion Proteins / metabolism
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Thionucleotides
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Transcription, Genetic / drug effects*
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Transfection
Substances
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Insulin
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RNA, Messenger
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Recombinant Fusion Proteins
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Thionucleotides
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8-((4-chlorophenyl)thio)cyclic-3',5'-AMP
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Dexamethasone
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Cyclic AMP
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Chloramphenicol O-Acetyltransferase
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Phosphoenolpyruvate Carboxykinase (GTP)