Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-17
pubmed:abstractText
RIG-G is a retinoic acid- or interferon-induced gene with potential anti-proliferation function. However, the mechanism underlying ATRA-induced RIG-G induction is not completely understood. Here, we demonstrate that ATRA up-regulates the expression of PU.1, which in turn directly binds to the promoter and increases the expression of RIG-G gene. Luciferase reporter assay and electrophoretic mobility shift assay reveal that PU.1 preferentially binds to one of the two putative binding sites on the RIG-G promoter. Moreover, silencing of PU.1 by shRNA markedly inhibited ATRA- but not IFN?-induced expression of RIG-G. These data provide new insight into the mechanism of ATRA-induced RIG-G expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1873-3468
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
21
pubmed:volume
585
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
375-80
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
PU.1 directly regulates retinoic acid-induced expression of RIG-G in leukemia cells.
pubmed:affiliation
Department of Pathophysiology and Chemical Biology, Division of Shanghai Universities E-Institutes, Key laboratory of Cell Differentiation and Apoptosis of Minister of Education, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't