Histone methylation by PRC2 is inhibited by active chromatin marks.
By F. Schmitges, A. B. Prusty, M. Faty, Alexandra Stützer, G. Lingaraju, J. Aiwazian, R. Sack, D. Hess, Ling Li, Shaolian Zhou and 12 more. Molecules and Cells, 2011
727 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/da6af82856463637c1bd8c2284beb5f9c5d20b90
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- D. Reinberg
- J. Simon
- Robert E. Kingston
- P. Voigt
- Wee-Wei Tee
- H. Stunnenberg
- Brian D. Strahl
- Scott B. Rothbart
Citations in the corpus
- A double take on bivalent promoters. (2013, background): “Importantly, whereas PRC2 cannot modify H3 copies that carry H3K4me3 (Schmitges et al. 2011; Voigt et al. 2012), it is yet to be analyzed whether H3K4 trimethylases can act on the H3 copies that carry H3K27me3.”
- Interpreting thelanguage of histone and DNA modifications (2014, background): “Consistent with this observation, it has been demonstrated that PRC2 cannot methylate H3K27 when H3K4me3 is present on the same tail [35, 97].”
- The interplay of histone modifications – writers that read (2015, unknown): “These variant complexes, such as the complex containing RING1B/PCGF1/RYBP/BCOR/ KDM2B, have been implicated in recruitment of PRC1 and have been shown to have higher H2AK119u1 activity compared with canonical PRC1 complexes [91,94].”
- The Transcriptional and Epigenomic Foundations of Ground State Pluripotency (2012, background): “It appears to be mutually exclusive with H3K36me3 (Figures 3A–3C and Figure S3F), in line with recent biochemical data showing thatPRC2activity is inhibitedbyactive marks including H3K36me3 (Schmitges et al., 2011).”
- Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, background): “The sites that mediate K4me3 and K36me2/K36me3 inhibitory inputs appear to reside in SU(Z)12 (Schmitges et al., 2011), but their relationship to the SU(Z)12 stimulatory site (Yuan et al., 2012) has not yet been defined.”