HDAC4
- Known as:
- HDAC4
- Catalog number:
- 000426A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HDAC4
Related genes to: HDAC4
- Gene:
- HDAC4 NIH gene
- Name:
- histone deacetylase 4
- Previous symbol:
- BDMR
- Synonyms:
- KIAA0288, HDAC-A, HDACA, HD4, HA6116, HDAC-4
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2015-09-11
Related products to: HDAC4
Related articles to: HDAC4
- Low vitamin D levels during pregnancy are associated with an increased risk of Gestational Diabetes Mellitus (GDM), potentially mediated by altered vitamin D metabolism. Cytochrome P450 family 24 subfamily A member 1 (CYP24A1) plays a key role in vitamin D catabolism, but its epigenetic regulation in GDM remains unclear. - Source: PubMed
Publication date: 2026/05/06
Milan K LAnuradha MRamkumar K M - 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 - Hyperthermic intraperitoneal chemotherapy (HIPEC) for colorectal peritoneal metastases relies primarily on DNA-damaging agents whose efficacy depends on sustained cytotoxic exposure. Whether brief treatment can induce durable transcriptional remodeling remains unclear. Mithramycin A (MA) is a GC-rich DNA-binding agent with transcriptional regulatory activity involving chromatin-associated pathways. Here, we investigated the molecular and functional consequences of a single 90-min HIPEC-mimetic MA exposure in colorectal cancer models. RNA sequencing revealed extensive and coordinated transcriptional remodeling, affecting a substantial fraction of expressed genes and producing a response qualitatively distinct from mitomycin C. MA selectively suppressed key chromatin-associated regulatory factors, including DNMT1, JARID2, and HDAC4, while coordinately activating canonical cyclin-dependent kinase inhibitors CDKN1A, CDKN1C, and CDKN2C. Gene set enrichment analysis demonstrated enrichment of G2/M checkpoint pathways and suppression of oncogenic gene networks. These molecular changes translated into sustained inhibition of clonogenic growth and activation of caspase-dependent apoptosis following drug washout, with hyperthermia potentiating apoptotic signaling. Collectively, these findings indicate that brief MA exposure induces selective modulation of chromatin regulators and durable transcriptional reorganization, supporting modulation of chromatin regulatory networks as a potential therapeutic strategy for HIPEC-based colorectal cancer therapy. - Source: PubMed
Publication date: 2026/04/17
Coburn-Flynn OliviaButchy M VirginiaGhanem YazidEmery RobertVerchio VincentKnapp KristenCollier JessicaJethi SahilSpitz Francis RZhang PingElbezanti Weam OthmanHong Young Ki - Cardiovascular disease (CVD) is a major cause of morbidity/mortality in juvenile-onset systemic lupus erythematosus (JSLE), yet no reliable tools exist to stratify CVD-risk. - Source: PubMed
Publication date: 2026/03/26
Peng JunjieDönnes PierreMcDonnell ThomasArdoin Stacy PSchanberg Laura ELewandowski Laura BJury Elizabeth CRobinson George ACiurtin Coziana - This study aims to investigate how emodin, an active component of , regulates macrophage polarization through the HDAC4/NF-[Formula: see text]B/CXCL12 pathway and impacts the progression of hepatocellular carcinoma (HCC). The inhibitory effect of emodin on M2 polarization was assessed by collecting conditioned cell culture medium from HepG2 cells and treating macrophages with emodin. Network pharmacology and other experiments were used to identify HDAC4 as a key target, and this was further validated through molecular docking, surface plasmon resonance (SPR), and Western blot analysis. Additional validation of the HDAC4/NF-[Formula: see text]B(p65)/CXCL12 axis regarding HCC progression was conducted using single-cell RNA sequencing and an HCC model. The results demonstrate that macrophages with HepG2 supernatant after treating, including emodin, tetrahydroxy stilbene glucoside and physcion, were added to reduce macrophage M2 polarization and inhibit HepG2 invasion and migration. Network pharmacology and protein analysis were used to discover the role of HDAC4 as the target of three drugs in HCC. The feasibility of emodin as a drug target for HDAC4 was explored through molecular docking simulation and SPR, and then verified through Western blot and nuclear plasma separation analysis. Likewise, the HDAC4/NF-[Formula: see text]B (p65) pathway reduces M2 polarization and inhibits the invasion and migration of HepG2. By using a single-cell sequencing database to predict the high expression of chemokines in HCC, and verifying the effect of emodin's ability to reduce M2 polarization and inhibit HepG2 invasion and migration via the HDAC4/NF-[Formula: see text]B (p65)/CXCL12 pathway, the results were likewise validated . This study elucidates the novel role of emodin in HCC progression and macrophage polarization, and demonstrates how emodin-mediated HDAC4 inhibition effectively attenuates HCC invasion and migration. - Source: PubMed
Publication date: 2026/04/25
Zhang Yi-QiongXu Yong-JieLi Hai-ZhiWang ShuangLi Cheng-ChengHuang Chang-Yu-DongShi Ya-ChunLi XingZhao Shu-YunZhu Li-YingPan Wei