Mammalian beta-polymerase promoter: phosphorylation of ATF/CRE-binding protein and regulation of DNA binding.
AUTOR(ES)
Englander, E W
RESUMO
The gene for the mammalian DNA repair enzyme DNA polymerase beta (beta-pol) is constitutively expressed in most cells, but is regulated in a tissue-specific fashion and can be induced in response to some types of DNA damaging agents. The promoter for the human beta-pol gene has been characterized and found to be TATA-less, but it does have multiple GC boxes and one ATF/CRE-binding site located within 50 residues 5' of the major mRNA start site. The ATF/CRE-binding site has been found to be essential for activity of the cloned promoter. We report that a bovine testes DNA-binding protein with specificity for the beta-pol promoter ATF/CRE-binding site is phosphorylated in vivo and contains several phosphorylation sites. Sequence specific DNA-binding by the purified protein is reduced when the natural protein is dephosphorylated or when it is hyperphosphorylated by protein kinase A (cKA) in vitro. These results suggest the possibility that phosphorylation systems may change binding of this ATF/CRE-binding protein to the beta-pol promoter and in turn modulate the promoter. Possible correlation of the results with transient expression activity of the cloned beta-pol promoter fusion gene was obtained in 293 cells. Cotransfection with a cKA expression plasmid to elevate phosphorylation was found to strongly reduce promoter activity.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=328336Documentos Relacionados
- Protein binding elements in the human beta-polymerase promoter.
- Transfected human beta-polymerase promoter contains a ras-responsive element.
- DNA damage response of cloned DNA beta-polymerase promoter is blocked in mutant cell lines deficient in protein kinase A.
- Induction of beta-polymerase mRNA by DNA-damaging agents in Chinese hamster ovary cells.
- Novikoff hepatoma deoxyribonucleic acid polymerase. Sensitivity of the beta-polymerase to sulfhydryl blocking agents.