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- Publisher
- Springer Journals
- Copyright
- Copyright © 1998 by Macmillan Magazines Ltd.
- Subject
- Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
- ISSN
- 0028-0836
- eISSN
- 1476-4687
- DOI
- 10.1038/27945
- Publisher site
- See Article on Publisher Site
Abstract
Evi-1 encodes a zinc-finger protein that may be involved in leukaemic transformation of haematopoietic cells 1,2,3,4,5 . Evi-1 has two zinc-finger domains, one with seven repeats of a zinc-finger motif and one with three repeats 6 , and it has characteristics of a transcriptional regulator 7 , 8 . Although Evi-1 is thought to be able to promote growth and to block differentiation in some cell types 9,10,11 , its biological functions are poorly understood. Here we study the mechanisms that underlie oncogenesis induced by Evi-1 by investigating whether Evi-1 perturbs signalling through transforming growth factor-β (TGF-β), one of the most studied growth-regulatory factors, which inhibits proliferation of a wide range of cell types 12 . We show that Evi-1 represses TGF-β signalling and antagonizes the growth-inhibitory effects of TGF-β. Two separate regions of Evi-1 are responsible for this repression; one of these regions is the first zinc-finger domain. Through this domain, Evi-1 interacts with Smad3, an intracellular mediator of TGF-β signalling 13 , thereby suppressing the transcriptional activity of Smad3. These results define a new function of Evi-1 as a repressor of signalling through TGF-β.
Journal
Nature – Springer Journals
Published: Jul 2, 1998