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Adenovirus DNA binding protein inhibits SrCap-activated CBP and CREB-mediated transcription. Virology 2003 Sep 01;313(2):615-21

Date

09/05/2003

Pubmed ID

12954226

DOI

10.1016/s0042-6822(03)00386-6

Scopus ID

2-s2.0-0041885345 (requires institutional sign-in at Scopus site)   4 Citations

Abstract

The SNF2-related CBP activator protein (SrCap) is a potent activator of transcription mediated by CBP and CREB. We have previously demonstrated that the Adenovirus 2 DNA Binding Protein (DBP) binds to SrCap and inhibits the transcription mediated by the carboxyl-terminal region of SrCap (amino acids 1275-2971). We report here that DBP inhibits the ability of full-length SrCap (1-2971) to activate transcription mediated by Gal-CREB and Gal-CBP. In addition, DBP also inhibits the ability of SrCap to enhance Protein Kinase A (PKA) activated transcription of the enkaphalin promoter. DBP was found to dramatically inhibit transcription of a mammalian two-hybrid system that was dependent on the interaction of SrCap and CBP binding domains. We also found that DBP has no effect on transcription mediated by a transcriptional activator that is not related to SrCap, indicating that our reported transcriptional inhibition is specific for SrCap and not due to nonspecific effects of DBP's DNA binding activity on the CAT reporter plasmid. Taken together, these results suggest a model in which DBP inhibits cellular transcription mediated by the interaction between SrCap and CBP.

Author List

Xu X, Tarakanova V, Chrivia J, Yaciuk P

Author

Vera Tarakanova PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Acetyltransferases
Adenosine Triphosphatases
Adenoviridae
Animals
CHO Cells
CREB-Binding Protein
Cricetinae
Cyclic AMP Response Element-Binding Protein
Cyclic AMP-Dependent Protein Kinases
DNA-Binding Proteins
Gene Expression Regulation
Membrane Proteins
Nuclear Proteins
Phosphoproteins
Protein Binding
Trans-Activators
Transcription, Genetic
Viral Proteins