한빛사 논문
Jia-Ray Yu1,2,5, Chul-Hwan Lee1,2,5, Ozgur Oksuz1,2,3,5, James M. Stafford1,2,4 and Danny Reinberg1,2,*
1 Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA; 2 Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA
Present addresses: 3 Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA; 4 Department of Neurological Sciences, University of Vermont Larner College of Medicine, Burlington, Vermont 05405, USA.
5 These authors contributed equally to this work.
*Corresponding author : Danny Reinberg
Abstract
As the process that silences gene expression ensues during development, the stage is set for the activity of Polycomb-repressivecomplex 2 (PRC2) to maintain these repressed gene profiles. PRC2 catalyzes a specific histone posttranslational modification(hPTM) that fosters chromatin compaction. PRC2 also facilitates the inheritance of this hPTM through its self-contained “writeand read” activities, key to preserving cellular identity during cell division. As these changes in gene expression occurwithout changes in DNA sequence and are inherited, the process is epigenetic in scope. Mutants of mammalian PRC2 or of itshistone substrate contribute to the cancer process and other diseases, and research into these aberrant pathways is yieldingviable candidates for therapeutic targeting. The effectiveness of PRC2 hinges on its being recruited to the proper chromatinsites; however, resolving the determinants to this process in the mammalian case was not straightforward and thus piqued theinterest of many in the field. Here, we chronicle the latest advances toward exposing mammalian PRC2 and its high maintenance.
Keywords : chromatin, epigenetics, PRC2, Polycomb
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