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Volume 271, Number 42, Issue of October 18, 1996 pp. 26007-26012
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

ELF-1 Interacts with and Transactivates the IgH Enhancer pi  Site

(Received for publication, May 15, 1996, and in revised form, July 26, 1996)

Yasmin Akbarali , Peter Oettgen , Jay Boltax and Towia A. Libermann

From the Department of Medicine, Beth Israel Hospital, and Harvard Medical School, Boston, Massachusetts 02215

We previously identified a B-cell-specific regulatory element in the immunoglobulin heavy chain (IgH) enhancer, pi , with striking similarity to binding sites for ets-related transcription factors. Whereas the ability of ets-related factors to bind to and transactivate the pi  site has been substantiated, the identification of the particular member of the ets family responsible for B-cell-specific regulation of the pi  site has remained controversial. We have used antibodies specific for individual members of the ets family to evaluate which ets-related factor in B-cell nuclear extracts interacts with the IgH pi  site. We present strong evidence that ELF-1 is highly expressed in B-cells and is one of two major factors specifically interacting with the murine IgH enhancer pi  site in B-cell nuclear extracts. Binding of ELF-1 correlates with activity of the pi  site, since mutations abolishing function of pi  also inhibit binding of ELF-1. Furthermore, we demonstrate that ELF-1 can transactivate the IgH enhancer in HeLa cells, suggesting a role for ELF-1 in B-cell-specific IgH gene expression.


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