Skip Navigation

This Article
Right arrow Print PDF (1212K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (24)
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by O'Neil, D.
Right arrow Articles by Bank, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O'Neil, D.
Right arrow Articles by Bank, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1990, Vol. 18, No. 8 1977-1982
© 1990

MOLECULAR BIOLOGY

Protein - DNA interactions upstream from the Human A gamma globin gene

David O'Neil*, James Kaysen, Maryann Donovan-Peluso, Madalyn Castle and Arthur Bank

Departments of Genetics and Development, Medicine and Pathology, Columbia University New York, NY 10032, USA

* To whom correspondence should be addressed at Department of Pathology, Columbia University, New York, NY 10032, USA

Received January 29, 1990. Revised March 7, 1990. Accepted March 7, 1990.

We have used DNAase I footprinting and the gel mobility shift assay to study proteins which bind to promoter elements located between –140 and –382 upstream of the human A gamma globin gene. Footprints are found with both erythroid and non-erythroid nuclear extracts at three sites: from –294 to –264, –242 to –227, and –189 to –172 from the transcription initiation site. An erythroid-specific footprint is identified from –194 to –189. We demonstrate that two known transcription factors, the ubiquitous octamer-bindlng protein OTF-1 and the erythroid regulatory factor NFE-1, bind to the –194 to –172 region and that their footprints overlap. Binding of OTF-1 to this region is reduced by a mutation at –175 associated with a form of non-deletion hereditary persistence of fetal hemoglobin. We conclude that OTF-1 may compete with NFE-1 for the –175 binding site, possibly functioning as a repressor of gamma globin transcription.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
L.-R. Liu, Z.-W. Du, H.-L. Zhao, X.-L. Liu, X.-D. Huang, J. Shen, L.-M. Ju, F.-D. Fang, and J.-W. Zhang
T to C Substitution at -175 or -173 of the {gamma}-Globin Promoter Affects GATA-1 and Oct-1 Binding in Vitro Differently but Can Independently Reproduce the Hereditary Persistence of Fetal Hemoglobin Phenotype in Transgenic Mice
J. Biol. Chem., March 4, 2005; 280(9): 7452 - 7459.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
D. O'Neill, J. Yang, H. Erdjument-Bromage, K. Bornschlegel, P. Tempst, and A. Bank
Tissue-specific and developmental stage-specific DNA binding by a mammalian SWI/SNF complex associated with human fetal-to-adult globin gene switching
PNAS, January 19, 1999; 96(2): 349 - 354.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
S. D. Langdon and R. E. Kaufman
Gamma-Globin Gene Promoter Elements Required for Interaction With Globin Enhancers
Blood, January 1, 1998; 91(1): 309 - 318.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
T. Ikuta, T. Papayannopoulou, G. Stamatoyannopoulos, and Y. W. Kan
Globin Gene Switching. IN VIVO PROTEIN-DNA INTERACTIONS OF THE HUMAN beta -GLOBIN LOCUS IN ERYTHROID CELLS EXPRESSING THE FETAL OR THE ADULT GLOBIN GENE PROGRAM
J. Biol. Chem., June 14, 1996; 271(24): 14082 - 14091.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.