Journal
NUCLEIC ACIDS RESEARCH
Volume 28, Issue 17, Pages 3370-3378Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/28.17.3370
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS030994] Funding Source: NIH RePORTER
- NINDS NIH HHS [R01 NS030994, NS30994] Funding Source: Medline
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High levels of transcription from the amyloid precursor protein promoter are dependent on the binding of CTCF to the APB beta core recognition sequence located between positions -82 and -93 upstream from the transcriptional start site, CTCF comprises 727 amino acids and contains 11 zinc finger motifs arranged in tandem that are flanked by 267 amino acids on the N-terminal side and 150 amino acids on the C-terminal side. Deletion of either the N- or the C-terminal regions outside of the zinc finger domain had no detrimental effect on the binding of CTCF to APB beta. However, internal deletions of zinc fingers 5-7 completely abolished binding. The binding of full-length CTCF generated a DNase I protected domain extending from position -78 to -116, which was interrupted by a hypersensitive site at position -99, Selective deletions from the N- and C-terminal sides of the zinc finger domain showed that the N-terminal end of the zinc finger domain was aligned toward the transcriptional start site, Furthermore, deletions of zinc fingers peripheral to the essential zinc fingers 5-7 decreased the stability of the binding complex by interrupting sequence-specific interactions.
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