Histone deacetylase inhibitors.
By C. Monneret. European journal of medicinal chemistry, 2005
991 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/adbac3d3e4bffec859b4e832ba47136a91cdbd2f
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
- PA Marks
- Weisheng Xu
- R. Parmigiani
- Guangdi Wang
- Tien L. Huang
- Madhusoodanan Mottamal
- Shilong Zheng
- Congcong He
In Oncology
Citations in the corpus
- Pharmacologic disruption of Polycomb-repressive complex 2-mediated gene repression selectively induces apoptosis in cancer cells. (2007, background): “Because DZNep produced a similar phenotype as that caused by HDACI in our cellular screening and PRC2-mediated gene repression depends on HDAC activity (van der Vlag and Otte 1999; Varambally et al. 2002), we explored the possibility that DNZep might interfere with PRC2 proteins and related histone ”
- Decreased histone deacetylase activity in chronic obstructive pulmonary disease. (2005, background): “Several molecules and genes have been identified or developed or both to inhibit HDACs.(3) Valproic acid, an antiepileptic drug that has been commercially available for decades, has been found to inhibit HDACs, including HDAC2.”
- Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “inhibition of HDACs would be advantageous over paninhibition of HDACs in cancer treatment (4, 50, 62).”
- Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation (2007, background): “TSA is a member of the hydroxamate class of HDAC inhibitors, which also includes suberoylanilide hydroxamic acid, pyroxamide, and Scriptaid (Marks et al., 2004).”
- Histone Deacetylase Inhibitors in Clinical Studies as Templates for New Anticancer Agents (2015, background): “The cap group, linker and the zinc binding domain (ZBD) are colored green, red and blue, respectively.”
- Discovery and development of SAHA as an anticancer agent (2007, background): “Class III HDACs, the socalled Sir2 family, are not inhibited by SAHA and do not have the same targets as class I and II deacetylases (Haggerty et al., 2003).”
- Regulation Mechanisms and Signaling Pathways of Autophagy (2009, background): “Various HDAC chemical inhibitors, including SAHA (suberoylanilide hydroxamic acid) and butyrate, promote hyperacetylation of histones and preferentially target cancer cells for both apoptotic and caspase-independent autophagic cell death in cell lines and animal models (89,135).”
- Histone deacetylase inhibitors: molecular mechanisms of action (2007, background): “HDACi have been discovered with different structural characteristics, including hydroximates, cyclic peptides, aliphatic acids and benzamides (Table 2) (Miller et al., 2003; Yoshida et al., 2003; Marks and Breslow, 2007).”
- Transmembrane transport of endo- and xenobiotics by mammalian ATP-binding cassette multidrug resistance proteins. (2006, background): “FK228 interferes with several transduction pathways and has most recently been demonstrated to be a potent inhibitor of histone deacetylase (344).”