Covalent histone modifications: miswritten, misinterpreted, and miserased in human cancers
By P. Chi, C. D. Allis, G. Wang. Nature Reviews. Cancer, 2010
1,105 citations recorded by the source corpus.
Post-translational modification of histones provides an important regulatory platform for processes such as gene transcription and DNA damage repair. It has become increasingly apparent that the misregulation of histone modification, which is caused by the deregulation of factors that mediate the modification installation, removal and/or interpretation, actively contributes to human cancer. In this Review, we summarize recent advances in understanding the interpretation of certain histone methylations by plant homeodomain finger-containing proteins, and how misreading, miswriting and mis-erasing of histone methylation marks can be associated with oncogenesis and progression. These observations provide us with a greater mechanistic understanding of epigenetic alterations in human cancers and might also help direct new therapeutic interventions in the future.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/989edad48ddbf3db615e9cdec19363b51392ec7b
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In Molecular Biology
- Manel Esteller
- Anna Portela
- Makoto Nakakido
- Howard Y. Chang
- Ryuji Hamamoto
- J. Tyler
- Manuel Rodríguez‐Paredes
- Charles J. David
Citations in the corpus
- Epigenetic modifications and human disease (2010, background): “Of the enzymes that modify histones, methyltransferases, histone demethylases and kinases are the most specific to individual histone subunits and residue”
- The LSD1 Family of Histone Demethylases and the Pumilio Posttranscriptional Repressor Function in a Complex Regulatory Feedback Loop (2015, background): “Dynamic posttranslational modifications of histones influence the accessibility of chromatin and the expression of transcripts (1).”
- Cancer epigenetics reaches mainstream oncology (2011, background): “Many MLL fusions seem to activate leukemia-promoting genes by abnormal recruitment of DOT1L, the non-SET-domain HMT for H3K79 (ref”
- DNA methylation: superior or subordinate in the epigenetic hierarchy? (2011, background): “Histone tails undergo a variety of covalent modifications including acetylation, methylation, phosphorylation, ubiquitination, and sumoylation, regulating key cellular process such as gene transcription, DNA replication, and DNA repair.(24,25) During mammalian development and cancer, DNA methylation”
- DANPOS: Dynamic analysis of nucleosome position and occupancy by sequencing (2013, background): “2009), as well as disease processes, such as cancer and aging (Chi et al. 2010; Feser and Tyler 2011; Zhang and Pugh 2011).”
- Histone Methylation Dynamics and Gene Regulation Occur through the Sensing of One-Carbon Metabolism (2015, background): “Genes that encode these enzymes are frequently altered in pathological states, leading to alterations in methylation (Chi et al., 2010; Dawson and Kouzarides, 2012).”
- Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged. (2010, background): “Each regulatory point in the control of gene expression (which includes chromatin structure, splicing and polyadenylation of mRNA precursors, translation, and mRNA and protein stability) is subject to profound alterations during the development of most, if not all, cancers (Venables 2006; Mayr and B”
- Long intergenic non-coding RNAs – New links in cancer progression (2011, background): “Epigenetic alterations are potentially stable and heritable and can occur at a much greater rate than DNA mutations in somatic cells (15).”
- MLL-rearranged Leukemia is Dependent on Aberrant H3K79 Methylation by DOT1L (2011, positive): “It has become increasingly clear that these enzymes are also critical for cancer development (Albert and Helin, 2010; Chi et al., 2010).”
- Lysine Glutarylation Is a Protein Post-Translational Modification Regulated by SIRT5 (2014, background): “These PTM enzymes have important roles in modulation of chromatin structure and transcriptional regulation (Berger, 2007; Chi et al., 2010).”