Article Information
History
- December 7, 2020.
Article Versions
- Version 1 (January 30, 2020 - 17:00).
- You are viewing Version 2, the most recent version of this article.
Copyright
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
Author Information
- Christopher M. Weber1,2,
- Antonina Hafner2,
- Simon M. G. Braun1,2,
- Jacob G. Kirkland1,2,
- Benjamin Z. Stanton3,4,5,
- Alistair N. Boettiger2 and
- Gerald R. Crabtree1,2,6,*
- 1Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
- 2Developmental Biology, Stanford University School of Medicine, Stanford, California, USA
- 3Nationwide Children’s Hospital, Center for Childhood Cancer and Blood Diseases, Columbus, Ohio, USA
- 4Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA
- 5Department of Biological Chemistry and Pharmacology, The Ohio State University College of Medicine, Columbus, Ohio, USA
- 6Howard Hughes Medical Institute, Chevy Chase, Maryland, USA
- ↵*Correspondence should be addressed to G.R.C. (crabtree{at}stanford.edu)
Posted December 07, 2020.
mSWI/SNF promotes polycomb repression both directly and through genome-wide redistribution
