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
- Amblyopia is a neurodevelopmental disorder for which effective treatments in adults are limited due to reduced cortical plasticity. Environmental enrichment (EE) can partially restore this plasticity, but the underlying molecular mechanisms remain unclear. This study investigated whether the miR-132/HDAC3 pathway is associated with EE-induced visual recovery in adult amblyopic mice. An adult amblyopia model (n = 64) was established via monocular deprivation (MD). Amblyopic mice were assigned to untreated, standard housing (SH), or EE groups, with normal mice as controls. Visual function was assessed using flash visual evoked potentials (fVEP), and molecular analyses of miR-132 and HDAC3 in the primary visual cortex (V1) were performed. In vitro studies included a dual-luciferase assay to verify miR-132-HDAC3 targeting and evaluated the effects of miR-132/HDAC3 overexpression on cortical neurons. Compared to SH, EE-reared amblyopic mice showed (1) increased N1-P2 wave amplitude in fVEP and (2) upregulated miR-132 and downregulated HDAC3 in V1. In vitro, HDAC3 was confirmed as a direct miR-132 target, and miR-132 overexpression suppressed HDAC3 while promoting structural remodeling in visual cortical neurons. These findings suggest that the miR-132/HDAC3 pathway potentially contributes to EE-induced visual restoration in adult amblyopia. - Source: PubMed
Ding SuzhenLi YongZhang YutongZhang TingyuLi Lan - Exercise promotes physiological cardiomyocyte growth and protects against ischaemia-reperfusion (IR) injury in the heart. The molecular mechanism by which exercise benefits cardiac metabolism and function remains largely unknown. Here, using a genetically encoded fluorescent sensor, we show that exercise increases cytosolic, but not mitochondrial, NADPH levels in cardiomyocytes. This effect is mediated by activation of the pentose phosphate pathway (PPP). Inhibition of PPP activity or depletion of cytosolic NADPH attenuates exercise-induced heart hypertrophy in mice. We observe that NADPH promotes cardiomyocyte growth by inhibiting HDAC3/C/EBPβ pathways. Moreover, exercise-activated PPP/NADPH pathway suppresses acute IR injury and preserves heart function 4 weeks after IR. Among 310 tested Tibetan compounds, the spermidine derivative lyciumspermidine-0527 directly activates the rate-limiting PPP enzyme glucose-6-phosphate dehydrogenase, elevates intracellular NADPH levels and alleviates IR injury. Altogether, these results show that PPP-derived NADPH is a critical metabolic checkpoint that regulates exercise-induced physiological cardiomyocyte growth and protects against IR-induced heart injury. - Source: PubMed
Publication date: 2026/09/08
Wu DanChen TaoDong XinLi HaoqiCheng ZijieLi HuiminChao YufanLi FanglingYin YunGuo FujunXu XinranZhang YuxuanNing KunFu XiaoqingBian YueminMa FenfenRitterhoff JuliaWang WangHu Qingxun - SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) is a key epigenetic regulator that catalyzes histone H3 lysine 9 trimethylation (H3K9me3), a mark essential for transcriptional repression and heterochromatin formation. Here, we investigated the role of SETDB1 during zygotic genome activation (ZGA) in porcine embryos. SETDB1 knockdown (KD) was induced by microinjecting double-stranded RNA (dsRNA), and its impact on early embryonic development was evaluated. SETDB1 KD decreased H3K9me3 levels, markedly increased H3K9ac, and downregulated ZGA-associated genes. These epigenetic alterations were accompanied by impaired cleavage, reduced blastocyst formation, and a lower total cell number. Upon etoposide-induced DNA double-strand breaks, SETDB1 KD embryos showed reduced expression of key DNA repair proteins, failed to efficiently restore DNA integrity, and exhibited increased apoptosis, indicating a compromised DNA damage response and repair process. SETDB1 KD also reduced HDAC3 expression, suggesting that SETDB1 may regulate HDAC3 to maintain histone acetylation balance. Consistently, HDAC3 inhibition increased H3K9ac, decreased H3K9me3, and reduced SETDB1 protein levels, supporting a reciprocal regulatory relationship. Together, these findings indicate that SETDB1 is important for porcine embryonic development by coordinating histone modifications and safeguarding genomic integrity during ZGA, and they suggest that the interplay between SETDB1 and HDAC3 constitutes a potentially important epigenetic axis for proper histone modification dynamics and developmental competence. - Source: PubMed
Song Hyeon-JiLee Song-HeeZhan Cheng-LinLu Qin-YueLee Gyu-HyunSim Jae-MinJo Yu-JinKim Ji-SuCui Xiang-Shun - Tumor immune evasion is a pivotal mechanism driving therapeutic resistance and poor prognosis in lung cancer. The interleukin-20 receptor β subunit (IL20RB) is implicated in chronic inflammation and oncogenesis, but its precise function and molecular basis in non-small cell lung cancer (NSCLC) require elucidation. - Source: PubMed
Publication date: 2026/08/31
Wang YanghaoLi GuoyuWang WeizhouZhang HengruiZhang YuDeng YajieMu SirongYuan SiyuTu YulinNi JiayiHe YongwenBian Li - Xenophagy is a selective autophagy process crucial for eliminating intracellular pathogens, yet its regulatory mechanisms remain poorly defined. In this study, acetylome profiling identifies dynamic acetylation of the xenophagy receptor NDP52 at K202, and its deacetylation enhances during Salmonella Typhimurium infection. Acetyltransferase CREBBP/KAT3A and deacetylase HDAC3 reciprocally regulate NDP52 K202 acetylation. Deacetylated NDP52 binds more strongly to ATG8 family proteins (MAP1LC3A/B and GABARAPL2), promotes autophagosome-lysosome fusion and pathogen degradation. Innate immune kinase TBK1 phosphorylates HDAC3 at S424, stabilizes it by inhibiting ubiquitination-dependent degradation, and this regulatory cascade links innate immunity to xenophagy. Liver-specific overexpression of deacetylation-mimetic NDP52 in mice reduces hepatic Salmonella Typhimurium burden, attenuates liver necrosis, and suppresses proinflammatory cytokines. This study uncovers a post-translational modification paradigm in xenophagy, where NDP52 acetylation dynamics fine-tune receptor function in antibacterial responses, highlighting the HDAC3-NDP52 axis as a potential therapeutic target for infectious diseases. - Source: PubMed
Publication date: 2026/09/02
Sun WeixiaWang LuqingZhu YifeiZhou YeYing LingxuanYang WenlanLiu ChenJiang XiaoxueLi XieCheng Xiawei