Linked Life Data

9665135

Source:http://linkedlifedata.com/resource/pubmed/id/9665135

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6688
pubmed:dateCreated
1998-7-20
pubmed:abstractText
Evi-1 encodes a zinc-finger protein that may be involved in leukaemic transformation of haematopoietic cells. Evi-1 has two zinc-finger domains, one with seven repeats of a zinc-finger motif and one with three repeats, and it has characteristics of a transcriptional regulator. Although Evi-1 is thought to be able to promote growth and to block differentiation in some cell types, 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-beta (TGF-beta), one of the most studied growth-regulatory factors, which inhibits proliferation of a wide range of cell types. We show that Evi-1 represses TGF-beta signalling and antagonizes the growth-inhibitory effects of TGF-beta. 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-beta signalling, thereby suppressing the transcriptional activity of Smad3. These results define a new function of Evi-1 as a repressor of signalling through TGF-beta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
394
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
92-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3.
pubmed:affiliation
The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't