Ask about this productRelated genes to: HDAC9 antibody
- Gene:
- HDAC9 NIH gene
- Name:
- histone deacetylase 9
- Previous symbol:
- -
- Synonyms:
- KIAA0744, HDAC, MITR, HD7, HDAC7B
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-06
- Date modifiied:
- 2015-09-11
Related products to: HDAC9 antibody
Related articles to: HDAC9 antibody
- Cellular senescence and mitochondrial dysfunction are prevalent in adipose tissues and disrupt metabolic homeostasis during aging, but the mechanisms are poorly understood. Here, we investigated the role of histone deacetylase 9 (HDAC9), an epigenetic regulator of adipogenic differentiation, in aging-related adipose tissue senescence and mitochondrial dysfunction. HDAC9 expression correlated positively with age in mouse adipose tissues. Compared to age-matched wild-type (WT) mice, Hdac9 knockout (KO) mice gained less weight and had reduced fat mass during aging, in conjunction with reduced senescence-associated beta-galactosidase (SABG) staining and expression of senescence markers in adipose tissues. Additionally, preadipocytes isolated from Hdac9 KO mice exhibited reduced baseline and stress-induced senescence compared to WT mice. Mechanistically, HDAC9 gene deletion resulted in coordinated upregulation of mitochondria-associated genes, in association with increased mitochondrial DNA content and adipose tissue mitochondrial oxygen consumption parameters (e.g., increased basal respiration, proton leak). Furthermore, thiosulfate sulfurtransferase (TST), whose downregulation is associated with mitochondrial dysfunction, was reduced in adipose tissues of aging mice and upregulated by HDAC9 gene deletion. Finally, silencing TST in preadipocytes upregulated expression of senescence markers and increased SABG staining. We conclude that deletion of HDAC9 ameliorates the development of adipose tissue senescence and mitochondrial dysfunction with aging, at least in part via upregulation of TST, suggesting that targeting HDAC9 may be a promising strategy to maintain healthy adipose tissue during aging. - Source: PubMed
Goo BrandeeAhmadieh SamahVeerapaneni PraneetShi HongKim David SOgbi MouradChouhaita RonnieCyriac NicoleCave StephenLiu LinglingZhang YongDu QuanshengKim Ha WonLei YunLu Xin-YunWeintraub Neal L - Mood stabilizers (MS) are the cornerstone of maintenance treatment for bipolar disorder. However, their mechanisms of action remain only partially understood. Increasing evidence suggests that MS may exert part of their therapeutic effects through epigenetic modulations. In this exploratory study, we investigated the effects of therapeutic concentrations of six MS - valproic acid (VPA), lithium, lamotrigine, risperidone, aripiprazole, and quetiapine - on the expression of 82 genes involved in DNA methylations and histone modifications in HeLa cells. After seven days of exposure, VPA induced the most extensive transcriptional changes, with differential expression of 17 out of 82 genes, predominantly involved in histone modifications (acetylation, methylation, phosphorylation, ubiquitination). Notably, VPA upregulated HDAC1, HDAC2, HDAC9, HDAC11, KDM5B, and PAK1 mRNA levels with fold-changes >1.3. Corresponding increased protein levels were observed only for KDM5B and PAK1. VPA also induced direct inhibition of total HDAC activity, unlike lithium and quetiapine. Lithium and quetiapine upregulated HDAC2 and ESCO1 mRNA levels. Lithium and quetiapine did not modify HDAC2 protein levels. Other MS showed no significant transcriptional effects at day 7. Overall, MS-induced transcriptional changes were mainly restricted to genes involved in histone modifications, with minimal effects on DNA methylation-related genes. These findings suggest that MS, particularly VPA, modulate the transcription of epigenetic machinery genes in HeLa cells. HDAC2 upregulation may represent a shared transcriptional response across several MS, although the absence of consistent protein-level changes warrants caution. These results are exploratory and require replication in more physiologically relevant models to determine their biological and clinical significance. - Source: PubMed
Publication date: 2026/04/08
Hennion VincentRathes ArthnaPuszkiel AlicjaBellivier FrankDecleves XavierFroelicher-Bournaud LéoEtain BrunoMarie-Claire Cynthia - Epigenetic regulation is a key determinant of the aging process, and its dysregulation contributes to cognitive aging and increased vulnerability to Alzheimer's disease (AD). As major regulators of epigenetic processes, histone deacetylases (HDACs) have emerged as potential therapeutic targets for cognitive enhancement in neurodegenerative diseases. However, the distinct roles of individual HDAC isoforms remain to be defined. Here, we report that HDAC9 is specifically expressed in neurons of human and mouse brains, and its expression declines with age. HDAC9 deficiency impairs cognitive function and synaptic plasticity in young mice. Selective deletion of HDAC9 in hippocampal CA1 neurons also induces cognitive impairment. In contrast, overexpression of HDAC9 in forebrain glutamatergic neurons preserves cognitive function in aged mice. Moreover, HDAC9 is also downregulated in the brain of AD mouse models, whereas neuronal overexpression of HDAC9 alleviates AD-related cognitive and synaptic deficits and reduces Aβ deposition. Together, these findings suggest neuronal HDAC9 is necessary and sufficient for maintaining cognitive and synaptic functions in the context of aging and AD. - Source: PubMed
Publication date: 2026/04/04
Lei YunChen YutingGuo MingPatel FlorikabenBai YuGoo BrandeeDu QuanshengWeintraub Neal LLu Xin-Yun - Over the past five decades, air pollution has posed a growing threat to human health, particularly affecting the respiratory system. This study aims to investigate the potential molecular mechanisms underlying the relationship between exposure to air pollutants and the development of COPD and to identify potential gene targets that may play a key role in this process. In this study, researchers used several publicly available databases to obtain target genes related to air pollutants and COPD, determine the overlapping genes between them and performed GO and KEGG enrichment analyses to elucidate the underlying mechanisms. Cross-validation was performed using multiple datasets from the Gene Expression Omnibus (GEO) database to screen out candidate targets, and molecular docking techniques were utilized to investigated molecular interactions between candidate targets and air pollutants. Candidate targets were subsequently validated and analyzed using immune cell infiltration analysis, single-cell transcriptome data, risk prediction model construction and clinical data to further elucidate their relationship with COPD. Findings suggest that HDAC9, DPP9 and KCNN4 are candidate targets of air pollutants that are potentially involved in COPD development. These results offer new insights into the potential molecular mechanisms linking air pollution exposure to COPD and underscore the need for further in-depth research on air pollution issues. - Source: PubMed
Song DongXie LinGao XuegeChen YushanZhong ChunjunLi HuicongZhan ShaofengLian Leshen - CEU-938, an innovative antimicrotubule prodrug bioactivated by cytochrome P450 1A1 (CYP1A1), represents a promising targeted alternative for cancer cells overexpressing this enzyme. To optimize its clinical utility and minimize off-target effects in breast cancer (BC) patients, this study aims to identify predictive biomarkers of CEU-938 efficacy. The antiproliferative activity of CEU-938 was assessed across a panel of 39 human breast cancer and non-tumorigenic cell lines. Differential expression analyses were subsequently performed to distinguish CEU-938-responsive from non-responsive cell lines using a threshold of 1000 nM. Candidate biomarkers identified through this approach were then validated by RT-qPCR and Western blot analyses. CEU-938 demonstrated marked and selective antiproliferative activity across molecular subtypes of human breast cancer, with efficacy observed in approximately 40% of triple-negative breast cancer (TNBC), 70% of estrogen receptor-positive (ER), and 80% of human epidermal growth factor receptor 2-positive (HER2) breast cancer cell lines, while sparing non-tumorigenic human breast cells (MCF 10A, MCF-12A, 184B5). Differential expression analysis identified five candidate biomarkers associated with CEU-938 responsiveness, namely, FOXA1 (log2-fold change (LFC) = 3.1), RAB25 (LFC = 3.8), RHOV (LFC = 2.9), PRKCH (LFC = 1.6), and HDAC9 (LFC = -1.7). Among these, FOXA1 and RAB25 robustly validated by RT-qPCR and Western blot analyses, showing strong inverse correlations with CEU-938 sensitivity (Spearman correlation coefficients of -0.82 and -0.61, respectively, at the protein level). The predictive value of FOXA1 and RAB25 was further confirmed by Western blot analyses in two independent breast cell line models, the non-responsive MCF-12A and the responsive MDA-kb2. Collectively, these findings identify FOXA1 and RAB25 as robust predictive biomarkers of response to CEU-938. Notably, FOXA1 and RAB25 are strongly implicated in breast cancer biology, and FOXA1 has been directly linked to the aryl hydrocarbon receptor (AHR), the main regulator of CYP1A1. These results position CEU-938 as a strong precision-therapy candidate that combines target selectivity, a favorable toxicity profile, and biomarker-enabled patient stratification, with potential clinical benefit in ER and HER2 enriched tumors, as well as a subset of TNBC. - Source: PubMed
Publication date: 2026/02/25
Bruxelles QuentinHamel-Côté GenevièveScott-Boyer Marie-PierOuellette VincentC-Gaudreault RenéDurocher FrancineDiorio CarolineDroit ArnaudFortin Sébastien