17-SWI-SNF review

17-SWI-SNF review - Published OnlineFirst October 20, 2009;

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2009;69:8223-8230. Published OnlineFirst October 20, 2009. Cancer Res Bernard Weissman and Karen E. Knudsen Perturbations in Cancer SWI/SNF Hijacking the Chromatin Remodeling Machinery: Impact of Updated Version 10.1158/0008-5472.CAN-09-2166 doi: Access the most recent version of this article at: Cited Articles http://cancerres.aacrjournals.org/content/69/21/8223.full.html#ref-list-1 This article cites 96 articles, 36 of which you can access for free at: Citing Articles http://cancerres.aacrjournals.org/content/69/21/8223.full.html#related-urls This article has been cited by 6 HighWire-hosted articles. Access the articles at: E-mail alerts related to this article or journal. Sign up to receive free email-alerts Subscriptions Reprints and . pubs@aacr.org Publications Department at To order reprints of this article or to subscribe to the journal, contact the AACR Permissions . permissions@aacr.org Department at To request permission to re-use all or part of this article, contact the AACR Publications American Association for Cancer Research Copyright © 2009 on February 2, 2011 cancerres.aacrjournals.org Downloaded from Published OnlineFirst October 20, 2009; DOI:10.1158/0008-5472.CAN-09-2166
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Review Hijacking the Chromatin Remodeling Machinery: Impact of SWI/SNF Perturbations in Cancer Bernard Weissman 1 and Karen E. Knudsen 2 1 Department of Pathology and Laboratory and Lineberger Cancer Center, University of North Carolina, Chapel Hill, North Carolina and 2 Department of Cancer Biology, Department of Urology, and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania Abstract There is increasing evidence that alterations in chromatin re- modeling play a significant role in human disease. The SWI/ SNF chromatin remodeling complex family mobilizes nucleo- somes and functions as a master regulator of gene expression and chromatin dynamics whose functional specificity is driv- en by combinatorial assembly of a central ATPase and associ- ation with 10 to 12 unique subunits. Although the biochemical consequence of SWI/SNF in model systems has been extensive- ly reviewed, the present article focuses on the evidence linking SWI/SNF perturbations to cancer initiation and tumor pro- gression in human disease. [Cancer Res 2009;69(21):8223 30] Introduction The SWI/SNF family of chromatin remodeling complexes are master regulators of transcription factor action and resultant gene expression programs. SWI/SNF complexes are large, 2-MDa mul- ti-subunit conglomerates that serve to either enhance or suppress gene transcription through mobilization of nucleosomes (1, 2). In- triguingly, mounting evidence supports the paradigm that specific- ity of SWI/SNF action evolves through combinatorial assembly of 10 to 12 subunits, and that imbalances in subunit composition are frequently observed in human cancers. Although the functions of SWI/SNF in transcriptional control and development have been extensively reviewed (1 6), the present study will focus exclusively
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17-SWI-SNF review - Published OnlineFirst October 20, 2009;

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