Topic
HDAC3
About: HDAC3 is a research topic. Over the lifetime, 377 publications have been published within this topic receiving 17100 citations. The topic is also known as: HD3 & RPD3.
Papers published on a yearly basis
Papers
TL;DR: These studies show that the second-generation HPCs, unlike HMBA, are potent inhibitors of HDAC activity, and appear to induce differentiation by different pathways.
Abstract: Hybrid polar compounds (HPCs) have been synthesized that induce terminal differentiation and/or apoptosis in various transformed cells. We have previously reported on the development of the second-generation HPCs suberoylanilide hydroxamic acid (SAHA) and m-carboxycinnamic acid bishydroxamide (CBHA) that are 2,000-fold more potent inducers on a molar basis than the prototype HPC hexamethylene bisacetamide (HMBA). Herein we report that CBHA and SAHA inhibit histone deacetylase 1 (HDAC1) and histone deacetylase 3 (HDAC3) activity in vitro. Treatment of cells in culture with SAHA results in a marked hyperacetylation of histone H4, but culture with HMBA does not. Murine erythroleukemia cells developed for resistance to SAHA are cross-resistant to trichostatin A, a known deacetylase inhibitor and differentiation inducer, but are not cross-resistant to HMBA. These studies show that the second-generation HPCs, unlike HMBA, are potent inhibitors of HDAC activity. In this sense, HMBA and the second-generation HPCs appear to induce differentiation by different pathways.
1,015 citations
TL;DR: It is shown that genomic recruitment of HDAC3 by Rev-erbα directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.
Abstract: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbα. Rev-erbα colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbα in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbα directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.
682 citations
TL;DR: NF-kappaB p65 subunit repressed the Nrf2-antioxidant response element (ARE) pathway at transcriptional level and might provide a new insight into a possible role of NF- kappaB in suppressing the expression of anti-inflammatory or anti-tumor genes.
652 citations
TL;DR: HDAC3 is identified as a gene deregulated in human colon cancer and as a novel regulator of colon cell maturation and p21 expression and it is suggested that the growth-inhibitory and apoptotic effects induced by HDAC inhibitors are probably mediated through the inhibition of multiple HDACs.
618 citations
TL;DR: In this article, the authors show that in liver, class IIa histone deacetylases (HDAC4, 5, and 7) are phosphorylated and excluded from the nucleus by AMPK family kinases.
566 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2026 | 1 |
| 2025 | 12 |
| 2024 | 26 |
| 2023 | 105 |
| 2022 | 75 |
| 2021 | 38 |