Cis-regulation of the L-type pyruvate kinase gene promoter by glucose, insulin and cyclic AMP.
AUTOR(ES)
Bergot, M O
RESUMO
The glucose/insulin response element of the L-pyruvate kinase gene is a perfect palindrome located from nt -168 to -144 with respect to the cap site. This element (L4) is partially homologous to MLTF binding sites. Its full efficiency requires cooperation with a contiguous binding site for HNF4, termed L3 and located from nt -145 to -125. In the presence of the L4 element contiguous to L3, cyclic AMP inhibits activity of the L-PK promoter while in its absence, or when the normal L4-L3 contiguity is modified, cyclic AMP behaves as a transcriptional activator that does not seem to be sequence-specific. Therefore, we propose that the mechanism of inhibition of the L-PK gene by cyclic AMP requires precise interactions between the nucleoprotein complex built up at sites L4 and L3 and other components of the L-PK transcription initiation complex.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=312300Documentos Relacionados
- Functional characterization of the L-type pyruvate kinase gene glucose response complex.
- Glucose and cAMP regulate the L-type pyruvate kinase gene by phosphorylation/dephosphorylation of the carbohydrate response element binding protein
- Elements responsible for hormonal control and tissue specificity of L-type pyruvate kinase gene expression in transgenic mice.
- Genetic regulation of galactokinase in Tetrahymena by cyclic AMP, glucose, and epinephrine
- Transcriptional regulation of the tyrosine hydroxylase gene by glucocorticoid and cyclic AMP.