You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Signal Transduction Convergence: Phorbol Esters and Insulin Inhibit Phosphoenolpyruvate Carboxykinase Gene Transcription Through the Same 10-Base-Pair Sequence
Richard M. O'Brien, Maria T. Bonovich, Claude D. Forest and Daryl K. Granner
Proceedings of the National Academy of Sciences of the United States of America
Vol. 88, No. 15 (Aug. 1, 1991), pp. 6580-6584
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2357340
Page Count: 5
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
Phosphoenolpyruvate carboxykinase (PEPCK) governs the rate-limiting step in gluconeogenesis. Glucocorticoids and cAMP increase PEPCK gene transcription and gluconeogenesis, whereas insulin and phorbol esters have the opposite effect. Insulin and phorbol esters are dominant, since they prevent cAMP and glucocorticoid-stimulated transcription. Basal promoter elements and hormone response elements for cAMP, glucocorticoids, and insulin have been defined in previous studies. By using stable transfectants containing a variety of different PEPCK-chloramphenicol acetyltransferase fusion gene constructs, a phorbol ester response sequence, located between positions -437 and -402 relative to the transcription start site, was identified. This region coincides with the insulin response sequence that has recently been defined in the PEPCK promoter. Using a vector containing various wild-type and mutated sequences of this region ligated to the heterologous thymidine kinase promoter, we delineated the boundaries of both elements to the 10 base pairs between positions -416 through -407. Thus, although it has been previously shown that insulin and phorbol esters repress PEPCK gene transcription through distinct pathways, the final target of insulin and phorbol ester action is the same DNA element.
Proceedings of the National Academy of Sciences of the United States of America © 1991 National Academy of Sciences