Histone deacetylase inhibitors: molecular mechanisms of action
By Weisheng Xu, R. Parmigiani, PA Marks. Oncogene, 2007
1,515 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/61dd2e2c5b664352f7be81c51abdc54c8dc032a3
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In Cellular and Molecular Neuroscience
In Molecular Biology
Citations in the corpus
- DZNep Is a Global Histone Methylation Inhibitor that Reactivates Developmental Genes Not Silenced by DNA Methylation (2009, background): “tors that affect the deacetylation of other proteins as well as histones, but are still successfully used in the treatment of cancer (23, 24).”
- Histone Deacetylase Inhibitors: Potential in Cancer Therapy (2009, methodology): “As a result, the cells show a transient arrest at prometaphase, followed by aberrant mitosis such as missegregation and loss of chromosomes, resulting in cell death by either apoptosis or, mitotic cell death/catastrophe [Xu et al., 2007].”
- Therapeutic application of histone deacetylase inhibitors for central nervous system disorders (2008, background): “Initially, this interest was precipitated by the discovery of the anticancer potential of HDAC inhibitor”
- The many roles of histone deacetylases in development and physiology: implications for disease and therapy (2009, background): “The exact mechanism for the effect of HDAC inhibitors on tumour cells is currently unknown, and numerous explanations, such as changes in gene transcription, direct induction of apoptosis, production of reactive oxygen species and induction of cell-cycle arrest, have been propose”
- HATs and HDACs: from structure, function and regulation to novel strategies for therapy and prevention (2007, background): “In the last article of this issue, Xu et al. (2007) review classical HDAC inhibitors as therapeutic agents and the molecular mechanisms of action.”
- Histone Deacetylase Inhibitors in Clinical Studies as Templates for New Anticancer Agents (2015, background): “In terms of its target, vorinostat inhibits Class I, II and IV HDAC proteins, but not the NAD+-dependent Class III HDAC [45–47].”