Polyclonal HDAC6
- Known as:
- Polyclonal HDAC6
- Catalog number:
- pc-366
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal HDAC6
Related genes to: Polyclonal HDAC6
- Gene:
- HDAC6 NIH gene
- Name:
- histone deacetylase 6
- Previous symbol:
- -
- Synonyms:
- KIAA0901, JM21, HD6, FLJ16239, PPP1R90
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2015-09-11
Related products to: Polyclonal HDAC6
Related articles to: Polyclonal HDAC6
- Histone deacetylase 6 (HDAC6) is a lysine deacetylase that modulates protein function and turnover, and is critically implicated in the pathogenesis of neurodegenerative disorders. [F]FSW-100 is a promising radioligand designed to enable visualization of HDAC6 in the brain. In this first-in-human PET study, we evaluated the clinical applicability of [F]FSW-100 by comprehensively assessing its safety profile, biodistribution, radiation dosimetry, and brain kinetics. - Source: PubMed
Publication date: 2026/06/15
Tago TetsuroSakata MuneyukiKamitaka YutoKameyama MasashiIshii KenjiToyohara Jun - Liver fibrosis is a common outcome of chronic liver injury and can progress to cirrhosis, yet effective anti-fibrotic therapies remain limited. Here, we identify histone deacetylase 6 (HDAC6) as the most consistently upregulated zinc-dependent HDAC in fibrotic livers and activated hepatic stellate cells (HSCs). However, systemic HDAC6 inhibition may be constrained by inefficient delivery to fibrogenic HSCs and increased off-target exposure. To enable selective HDAC6 inhibition in activated HSCs, we developed an activated HSC membrane-camouflaged PLGA nanomedicine (PLGA-Ric@HSCM) loaded with the HDAC6 inhibitor ricolinostat (Ric). Membrane cloaking preserves key adhesion and recognition proteins, promotes homotypic uptake by HSCs, and reduces macrophage sequestration in vivo. PLGA-Ric@HSCM dampened profibrotic transcriptional programs by restoring microtubule acetylation and suppressing both the canonical TGFβ/Smad2/3 pathway and the p38/c-JUN/ATF2 axis. Compared to PLGA-Ric, PLGA-Ric@HSCM shows a more pronounced reduction in fibrosis burden and improved hepatic pathology across etiologically distinct models. Together, PLGA-Ric@HSCM provides a biomimetic, HSC-targeted strategy to reprogram acetylation homeostasis via HDAC6 inhibition and consequently mitigate liver fibrogenesis. - Source: PubMed
Publication date: 2026/06/14
Yu LinZhang LuGao LuluHuang SiyueQin XueyingWang ZiruiLi SiqiMei ChunyanZhang MaolinZhang YaojingWang WeiWu MinLiu Jingjing - Chronic myeloid leukemia (CML) is driven by the BCR-ABL1 fusion oncoprotein and is managed with tyrosine kinase inhibitors (TKIs). However, resistance and persistence of leukemic stem/progenitor cells remain major clinical challenges. Autophagy-mediated survival signaling contributes to therapeutic resistance in CML. We hypothesized that histone deacetylase 6 (HDAC6), a key regulator of protein homeostasis and autophagic flux, is a therapeutic target in this context. Transcriptomic analysis of CML bone marrow datasets revealed enrichment of HDAC6-associated autophagy and stress-response gene programs. The selective HDAC6 inhibitor 7b induced sustained α-tubulin acetylation at lower concentrations than ricolinostat or nexturastat A. 7b reduced primary CML PBMC viability while sparing healthy PBMCs and was active in vivo. Combining 7b with the allosteric BCR-ABL1 inhibitor asciminib synergistically suppressed cell viability and clonogenic growth. A tandem mCherry-GFP-LC3 reporter showed that 7b blocks autophagosome maturation, thereby decreasing autophagic degradation. Cotreatment engaged a maladaptive integrated stress response (ISR), characterized by eIF2α phosphorylation, ATF4 and CHOP induction, MCL-1 suppression, PUMA and NOXA upregulation, and BCL-xL-dependent mitochondrial apoptosis, accompanied by caspase-2 activation. ISR activation occurred downstream of the autophagy disruption: rapamycin attenuated ISR activation, whereas ATG7 silencing intensified ISR signaling and apoptosis. CHOP knockdown blunted the BCL-xL/PUMA/NOXA shift and caspase-3 cleavage, establishing CHOP as required. Caspase-10 acted upstream of caspases-9, -7, and -3. The combination elicited immunogenic cell death markers: calreticulin exposure, ATP and HMGB1 release, elevated TNF-α, and reduced IL-8. These findings identify HDAC6-driven autophagy as a therapeutically exploitable vulnerability in CML that, when combined with asciminib, triggers ISR-dependent immunogenic apoptosis. - Source: PubMed
Publication date: 2026/06/12
Paik Ji YeonGajulapalli Sruthi ReddyLi VladimirPark SujungLee YejinOrlikova-Boyer BarboraLorant AnneChristov ChristoKirsch GilbertKang Hyoung JinSchnekenburger MichaelCerella ClaudiaDiederich Marc - Diabetic kidney disease (DKD) lacks specific biomarkers reflecting the interplay between mitochondrial dysfunction and immune microenvironment remodeling. To address this, we integrated multi-dataset transcriptomics (GEO, MitoCarta 3.0, GeneCards) with Weighted Gene Co-expression Network Analysis, protein-protein interaction networks, and machine learning algorithms to identify key diagnostic genes. Single-nucleus RNA sequencing was utilized to map cell-type distributions. Subsequently, a single-center cohort of 70 biopsy-confirmed DKD patients was enrolled for validation of the key hub gene, . We identified four hub genes: (downregulated), , , and (upregulated). All genes exhibited robust diagnostic efficacy, and single-nucleus analysis revealed distinct renal cell-type enrichment patterns. Clinically, high renal HDAC6 expression correlated with severe interstitial inflammation, elevated complement C3 and cystatin C, and reduced urinary ammonium (a clinical proxy for proximal tubular mitochondrial dysfunction). Crucially, high HDAC6 served as an independent risk factor for both renal endpoints and cardiorenal composite events. In conclusion, , , , and are key regulators in DKD. Specifically, intrarenal HDAC6 quantification serves as a precise histological metric for prognostic stratification and underscores its potential as a therapeutic target for DKD intervention. - Source: PubMed
Publication date: 2026/05/23
Duan SuyanZhou QianShi YingYe YuyouHua HujiaLiu DehuiXue YuqianZhang ChengningYuan YanggangXing ChangyingMao HuijuanZhang Bo - cGAS overactivation is linked to various inflammatory and autoimmune diseases. Recent studies identify HDACs as critical regulators of cGAS, suggesting that dual cGAS/HDAC inhibition could be a novel therapeutic strategy. Herein, we report the identification of an HDAC/cGAS dual inhibitor, containing a hydroxamic acid moiety. This compound exhibited potent inhibitory activity against human and mouse cGAS (IC: 0.17 and 1.80 μM, respectively) and moderate activity against HDAC3 and HDAC6 (IC: 1.2 and 0.4 μM, respectively). Mechanistically, directly suppresses cGAS activity and increases its acetylation levels via HDAC3 inhibition. This dual-action profile resulted in robust therapeutic efficacy in murine models of inflammatory bowel disease and Aicardi-Goutières syndrome. Collectively, represents the first cGAS/HDAC dual inhibitor, offering a promising lead for further investigation into cGAS-dependent disorders. - Source: PubMed
Publication date: 2026/06/10
Zhou ZihuaChen MingjieLei ShuyueWang MengDing ChunyongSong ZilanTang WeiZhang Ao