Ask about this productRelated genes to: HDAC3 Blocking Peptide
- Gene:
- HDAC3 NIH gene
- Name:
- histone deacetylase 3
- Previous symbol:
- -
- Synonyms:
- RPD3, HD3, RPD3-2, KDAC3
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-29
- Date modifiied:
- 2019-02-19
Related products to: HDAC3 Blocking Peptide
Related articles to: HDAC3 Blocking Peptide
- The shared and disease-specific mechanisms across the immune-mediated inflammatory diseases (IMIDs) spectrum remains incompletely characterized, despite the recognized role of autoantibodies as important indicators of immune tolerance breakdown and immune dysregulation. - Source: PubMed
Bai ZhouYu BomiaoWei ZimoXiao PanchengZhan MinghuaLi ManshengWang FangCheng YongjingZhao MinshuZhang ChaoZhang XuanYu XiaoboLiu Yudong - To investigate the impact of myomectomy on key endometrial receptivity genes: LIF, HOXA10, and HDAC3. - Source: PubMed
Publication date: 2026/07/26
Mikkelsen Thea FalkenbergVera-Rodríguez MaríaFedorcsák ZsofiaGreggains GarethFedorcsák PéterHald Kirsten - The DNA/RNA helicase Schlafen11 (SLFN11) is considered a sensitivity marker of various tumor cells for cytotoxic treatment with DNA damaging agents (DDA), such as cisplatin and PARP inhibitors (PARPi). Cells can epigenetically silence SLFN11 expression to gain chemoresistance, which can be targeted by HDAC inhibitors (HDACi). Here, we investigate the predictive value of SLFN11 expression for the response to three different PARPi in ovarian cancer cells. Furthermore, we target its epigenetic downregulation via HDACi for sensitization to cisplatin and PARPi. We show that HDAC3 plays a key role in SLFN11 silencing in W1 and W1CR ovarian cancer cells, confirmed by an HDAC3 knockdown approach. Therefore, addressing HDAC3 by novel class I HDACi DS-103 and FL-007 at non-toxic concentrations restored SLFN11 expression with various consequences for DDA treatment in W1, W1CR, and SKOV-3 cells. While DS-103 and FL-007 significantly sensitized cisplatin-resistant W1CR cells to cisplatin to the level of W1 cells, the response to various PARPi remains divergent. Whereas both HDACi induced significant sensitization in W1 and W1CR cells, and DS-103 in SKOV-3 cells for niraparib cytotoxicity, cells remain unaffected in response to olaparib and rucaparib. Both compounds were also shown to be less dependent on, or independent of, SLFN11 in different ovarian cancer cells. In sum, the first time reported functional link of HDAC3 and SLFN11 appears an attractive co-treatment opportunity of DDA with HDACi. This is particularly promising for niraparib as it has a broader approval independent of BRCA status compared to other PARPi. - Source: PubMed
Publication date: 2026/08/18
Eichhorn Julia MMenning JasminSchäker-Hübner LindaHansen Finn KKönig PhilippBendas Gerd - Embryonic stem cells (ESCs) are refractory to inflammatory stimuli but acquire inflammatory competence upon differentiation, yet the underlying mechanisms remain unclear. Here, we report that H2BK5ac regulates the acquisition of inflammatory potential in mouse ESCs during differentiation. H2BK5ac levels increased at the regulatory regions of inflammatory genes upon differentiation, and this modification was required for their transcriptional upregulation. An acetylation-deficient H2BK5A mutant impaired the upregulation of inflammatory genes, whereas an acetylation-mimicking H2BK5Q mutant had the opposite effect. We identified p300 and HDAC3 as the acetyltransferase and deacetylase, respectively, that control H2BK5ac: p300 protein levels increased upon differentiation and its depletion reduced H2BK5ac levels, whereas loss of HDAC3 increased H2BK5ac levels despite its unchanged protein levels. H2BK5Q overexpression in mouse embryos increased embryonic mortality and inflammatory cytokine secretion, consistent with its pro-inflammatory effect. Thus, our study reveals H2BK5ac as a regulator that establishes inflammatory potential in mouse ESCs during differentiation. - Source: PubMed
Publication date: 2026/08/12
Xi YanPei Shuai-ShuaiLou Qian-QianLi ShengZhang Bo-WenFeng Hong-YuWang YuXu Qian-RuYan Jing-JingHou JunqingZhang Lei-GuangYang LuSun JinChen Su - This study aimed to determine whether Polygonatum cyrtonema polysaccharides (PCP) protect against sleep deprivation (SD)-induced neurobehavioral disorders via gut microbiota and epigenetic regulation. PCP was characterized as a structurally stable, glucose-rich heteropolysaccharide. Intervention with PCP significantly alleviated anxiety- and despair-like behaviors, yielding a 42.7% improvement in open-arm exploration time during the EPM test compared to the SD group. Mechanistically, PCP preserved intestinal and blood-brain barrier integrity, suppressed microglial activation, and repaired hippocampal synapses. Microbial profiling revealed that PCP reshaped the gut microbiota by enriching butyrate-producing taxa, leading to a 1.3-fold elevation in fecal butyrate levels. This metabolic shift suppressed hippocampal HDAC3 activity and drove a 60.8% increase in BDNF expression. Notably, these neuroprotective effects were completely abolished in microbiota-depleted mice. Overall, PCP relies on a microbiota-driven cascade of butyrate production and subsequent epigenetic regulation to maintain gut-brain homeostasis. - Source: PubMed
Chen YiliGong XinrongChen YoumengCheng KejunZhang Xin