To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

DDIT3/CHOP and the sarcom… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

DDIT3/CHOP and the sarcoma fusion oncoprotein FUS-DDIT3/TLS-CHOP bind cyclin-dependent kinase 2.

Journal article
Authors Christoffer Bento
Mattias K Andersson
Pierre Åman
Published in BMC cell biology
Volume 10
Issue 1
Pages 89
ISSN 1471-2121
Publication year 2009
Published at Institute of Biomedicine, Department of Pathology
Pages 89
Language en
Subject categories Medical and Health Sciences, Cell and Molecular Biology, Cell biology


ABSTRACT: BACKGROUND: The DDIT3 gene encodes a transcription factor belonging to the CCAAT/enhancer binding protein (C/EBP) family. It is normally expressed at very low levels but is activated by cellular stress conditions and induces G1-arrest and, in some cell types, apoptosis. DDIT3 is found as a part of the fusion oncogene FUS-DDIT3 that is causal for the development of myxoid/round-cell liposarcomas (MLS/RCLS). RESULTS: In the present study, we searched for putative interaction partners of DDIT3 and the oncogenic FUS-DDIT3 among G1 cyclins and cyclin-dependent kinases. We found that FUS-DDIT3 and the normal DDIT3 bind CDK2. In addition, CDK2 showed an increased affinity for cytoskeletal proteins in cells expressing FUS-DDIT3 and DDIT3. CONCLUSIONS: We conclude that DDIT3 binds CDK2 and that many of the observed biological effects of DDIT3 may involve interaction with CDK2.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?