Cyclic AMP response element-binding protein, CRE-BP1, mediates the E1A-induced but not the Tax-induced trans-activation.

Abstract

The adenovirus E1A protein and tax protein (Tax) of human T-cell leukemia virus-1 (HTLV-1) are transcriptional regulators that do not bind to DNA directly. The ATF sites/CRE (cyclic AMP response element) of the adenovirus E4 promoter and the long terminal repeat of HTLV-1 have been shown to be required for E1A and Tax inducibility, respectively. Using the c-Myb-CRE-BP1 fusion protein, it was shown that CRE-BP1, which could bind to the ATF sites/CRE, mediated the E1A-induced trans-activation. For this activation, the N-terminal portion of CRE-BP1, which contained the putative metal finger structure, was essential but not sufficient. In contrast, the trans-activation induced by HTLV-1 Tax was not mediated by CRE-BP1. These results strongly suggested that E1A activates transcription through interaction with CRE-BP1, but another CRE-binding protein participates in the Tax-induced trans-activation.

• Authors: T Maekawa, S Matsuda, J Fujisawa, M Yoshida, S Ishii
• Journal: Oncogene (Oncogene) Vol. 6 Issue 4 Pg. 627-32 (Apr 1991) ISSN: 0950-9232 [Print] England
• PMID: 1827668 (Publication Type: Journal Article)

Chemical References

• Adenovirus Early Proteins
• Cyclic AMP Response Element-Binding Protein
• DNA-Binding Proteins
• Gene Products, tax
• Oncogene Proteins, Viral
• Proto-Oncogene Proteins
• Proto-Oncogene Proteins c-myb
• Transcription Factors
• Viral Fusion Proteins

Topics

• Adenovirus Early Proteins
• Chromosome Mapping
• Cyclic AMP Response Element-Binding Protein
• DNA-Binding Proteins (pharmacology)
• Gene Expression Regulation, Neoplastic
• Gene Products, tax
• In Vitro Techniques
• Oncogene Proteins, Viral
• Plasmids
• Promoter Regions, Genetic
• Proto-Oncogene Proteins (pharmacology)
• Proto-Oncogene Proteins c-myb
• Transcription Factors
• Transcriptional Activation (drug effects)
• Transfection
• Viral Fusion Proteins