Histone deacetylase (HDAC) inhibitor activation of p21WAF1 involves changes in promoter-associated proteins, including HDAC1.

By C. Gui, L. Ngo, Weisheng Xu, V. Richon, PA Marks. Proceedings of the National Academy of Sciences of the United States of America, 2004

600 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/03daf60154ea0dfa08ca462ed05c03fe7b62edf1

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In Molecular Biology

1. PA Marks
2. W-S Xu
3. Manel Esteller
4. S. Ropero
5. Weisheng Xu
6. R. Parmigiani
7. Pier Giuseppe Pelicci
8. S. Minucci

Citations in the corpus

• Lost in transcription: p21 repression, mechanisms, and consequences. (2005, background): “expression was apparent again when it was seen that suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, was able to down-regulate c-Myc levels and simultaneously increase p21 levels in multiple myeloma cells (35).”
• Histone deacetylase inhibitors: molecular mechanisms of action (2007, background): “HDAC inhibitors (HDACi) selectively alter gene transcription, in part, by chromatin remodeling and by changes in the structure of proteins in transcription factor complexes (Gui et al., 2004).”
• Histone Deacetylase Inhibitors: Potential in Cancer Therapy (2009, background): “The basis for the gene selective action of HDAC inhibitor in altering transcription is not well understood and may be determined, in part, by the composition of the transcription factor protein complexes [Gui et al., 2004].”
• HDAC family: What are the cancer relevant targets? (2009, background): “H4, acetylation of lysines 9 and 14 of histone H3, and methylation of lysine 4 of histone 3 in the p21Waf1/Cip1 promoter region [102].”
• Discovery and development of SAHA as an anticancer agent (2007, background): “The p21 gene is a direct target of SAHA (Gui et al., 2004).”
• Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy (2012, methodology): “To measure validated biomarkers of VOR effect in the PBMCs of patients, we performed parallel assays of total cellular histone acetylation and measured histone acetylation by chromatin immunoprecipitation (ChIP) at the human p21 gene promoter, a gene known to upregulate chromatin acetylation after V”
• Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, background): “Strikingly, both hyper-acetylation of chromatin at the CDKN1A (which encodes p21) promoter and transcriptional activation of CDKN1A occur at the same level in wild-type and p53-null cells, implying that hyper-acetylation of p53 is not important for the therapeutic efficacy of HDACi (although ace”
• The role of histone deacetylases (HDACs) in human cancer (2007, background): “In some tumors, p21WAF1 is epigenetically inactivated by hypoacetylation of the promoter, and treatment with HDAC inhibitors leads to the inhibition of tumor-cell growth and an increase in both the acetylation of the promoter and gene expression (Gui et al., 2004).”