Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 23, Issue 19, Pages 6901-6908Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.23.19.6901-6908.2003
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Funding
- NCI NIH HHS [P01 CA022443, CA-22443, CA-07175, T32 CA009614, T32-CA-009614-13] Funding Source: Medline
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Transient-transfection assays have been used to identify transcription factors, and genetic analyses of these factors can allow a dissection of their mechanism of activation. Epstein-Barr nuclear antigen 1 (EBNA-1) has been shown to activate transcription from transfected templates, but its ability to activate transcription from nuclear templates has been controversial. We have established cells with integrated EBNA-1-responsive templates and have shown that EBNA-1 activates transcription from these chromatin-embedded templates dose dependently. A mutational analysis of EBNA-1 has identified a domain required for transcriptional activation of integrated templates, but not of transfected templates. The ability of EBNA-1 to activate transcription from both integrated and transfected templates can be inhibited by a derivative of EBNA-1 lacking the amino acids required for activation from integrated templates. EBNA-1's mode of activating transfected templates is therefore genetically distinct from that acting on integrated templates.
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