Ask about this productRelated genes to: HDAC5 antibody
- Gene:
- HDAC5 NIH gene
- Name:
- histone deacetylase 5
- Previous symbol:
- -
- Synonyms:
- KIAA0600, NY-CO-9, FLJ90614
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2016-10-06
Related products to: HDAC5 antibody
Related articles to: HDAC5 antibody
- Microglia's role in epilepsy through neuroimmune communication is poorly understood. Mechanisms by which neurons activate microglia and how microglia affect neuronal activity to drive seizure-related inflammation remain unclear. Here, we elucidated a crucial axis connecting pathological adenosine triphosphate (ATP) release induced by epileptiform neuronal activity to microglial MEF2A-dependent hyperactivation, which exacerbates epilepsy pathology. In epilepsy models, seizures cause excessive ATP release, activating microglial P2X7 receptors, causing CAMKII phosphorylation. This triggers HDAC5 translocation, freeing MEF2A for acetylation, and enhancing transcription. Acetylated MEF2A increases CD74 and NEK7 expressions, enhancing NLRP3 inflammasome activation and microglial hyperactivation, worsening neuronal hyperexcitability by increasing inhibitory synapses clearance. Targeting microglial MEF2A with parecoxib or AAV knockdown reduced seizure severity and cognitive deficits and maintained synaptic inhibition by reducing excessive microglial phagocytosis. This reveals an ATP-P2X7-Ca⁺- MEF2A signaling axis connecting neuronal injury with pathogenic microglial activation, suggesting MEF2A as a therapeutic target for microglial-neuronal homeostasis restoration in epilepsy pathology. - Source: PubMed
Publication date: 2026/05/22
Wu JinghengFu JiayuanyuanWang ShuaiWu YuzhangWang XuFeng ShangangShi QiWang YuhaoShi YetongFang YehongLan YuWu QiaoliDu ChuanYin ShaoyaXu LixiaYan Hua - This study explores the molecular mechanism of HDAC5 in ferroptosis of intestinal epithelial cells in sepsis-induced acute intestinal injury. - Source: PubMed
Publication date: 2026/05/19
Zhu Jin-PengSun Mei-NaLiu Shi-HuiDu Zhi-An - Central nervous system (CNS) injury is a leading cause of death and long-term disability worldwide. Neurological deficits reflect disruption of central neural circuits. A major barrier to circuit repair is the intrinsically low regenerative potential of adult CNS neurons-linked in part to failure of injury-induced nuclear export of class IIa histone deacetylases (notably HDAC5)-together with a hostile post-injury microenvironment. Here we present a multifunctional nanosystem, encapsulating the class IIa HDAC4/5-selective inhibitor LMK-235 and featuring an electroactive polyaniline coating with asymmetrically distributed 5-hydroxytryptamine moieties. Upon reaching the lesion, our nanosystem assembles into large-pore scaffolds that (i) inhibit the activity of nuclear-retained class IIa HDACs in neurons and thereby reactivate intrinsic regenerative programs, (ii) regulate microglial activation to mitigate neuroinflammation, and (iii) provide an electroactive interface promoting activity-dependent synaptic reconnection. This multi-pronged approach illustrates an integrated platform with translational potential for CNS disorders in which circuit disconnection constrains recovery. - Source: PubMed
Publication date: 2026/05/04
Tong ShiqiangYe ShuaiMa FenfenXie XiaoyingSun YinzheMa ChuchuShi TiantianCheng ZhengLi ChangHan WeiliXie LaozhiZhou SongleiGong JianingHuang ChenHuang YukunJiang GanLiu XiaolinLi BingZeng FengGong JingruWang ZhihuaGao XiaolingMei QiyongLi Wei-GuangChen Jun - The glucocorticoid receptor (GR) is a ligand-activated transcriptional regulator that translocates from the cytoplasm to the nucleus and modulates gene expression by binding DNA elements and recruiting coregulators. Synthetic glucocorticoids promote osteoclast overactivation, but the transcriptional mechanisms in osteoclast precursors remain incompletely defined. In glucocorticoid-stimulated monocytes, the leucine-rich repeat-containing G-protein-coupled receptor 4 (LGR4), a gene inhibiting osteoclastogenesis, is significantly repressed and osteoclast differentiation genes are upregulated. In our previous work, we found that classical monocytes contribute to osteoclastogenesis and display low expression of LGR4. However, the underlying mechanism has not been fully elucidated. In this study, we show that the glucocorticoid receptor occupies a negative glucocorticoid response element (nGRE) within the LGR4 promoter and recruits histone deacetylase 4 (HDAC4), thereby repressing LGR4 transcription and enhancing osteoclast differentiation programs. These findings suggest that disrupting GR-HDAC4-mediated repression of LGR4 may provide a strategy to mitigate glucocorticoid-enhanced osteoclastogenesis. - Source: PubMed
Publication date: 2026/03/31
Fang QihangChen BinyuLu ShengdiLi GanChen DongSong WenqiZhu QiDing PengZhu DaoyuGao YoushuiLiu Pei - Impaired clearance of amyloid-β (Aβ) is a major pathological hallmark of Alzheimer's disease (AD). Although histone deacetylase (HDAC) inhibitors show therapeutic potential, their clinical translation for AD is hampered by poor blood brain barrier (BBB) penetration and an incomplete understanding of their mechanism in Aβ clearance. Here, angiopep2-conjugated nanoparticles (SAHA@LIPO-ANG2) for efficient BBB translocation and delivery of the HDAC inhibitor vorinostat (SAHA) was developed and its underlying mechanisms were validated. - Source: PubMed
Publication date: 2026/04/03
Huang NingningHong RuiCui XiaoyuCao LijunShi LiChen BinSu YixuanXu XinruHua ChenYing Tao