Abstract
Chd5 is an essential factor for neuronal differentiation and spermatogenesis and is a known tumor suppressor. H3K27me3 and H3K4un are modifications recognized by Chd5; however, it remains unclear how Chd5 remodels chromatin structure. We completely disrupted the Chd5 locus using the CRISPR-Cas9 system to generate a 52 kbp long deletion and analyzed Chd5 function in mouse embryonic stem cells. Our findings show that Chd5 represses murine endogenous retrovirus-L (MuERV-L/MERVL), an endogenous retrovirus-derived retrotransposon, by regulating H3K27me3 and H3.1/H3.2 function. J. Cell. Biochem. 117: 780-792, 2016.
Original language | English |
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Pages (from-to) | 780-792 |
Number of pages | 13 |
Journal | Journal of Cellular Biochemistry |
Volume | 117 |
Issue number | 3 |
DOIs | |
Publication status | Published - Mar 2016 |
All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology
- Cell Biology