HDAC5
- Known as:
- HDAC5
- Catalog number:
- 000549A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HDAC5
Related genes to: HDAC5
- 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
Related articles to: HDAC5
- The primary mechanisms driving UV-induced carcinogenesis include DNA damage leading to mutations, and reactive oxygen species (ROS) formation that can cause inflammation, immunosuppression, alteration of the structure of proteins, including transcription factors, and carcinogenesis through epigenetic modifications. Curcumin has the potential to inhibit DNA-methyltransferases (DNMTs) and histone deacetylases (HDACs), but this has not been examined yet at the gene-expression level. In this article, we aimed to explore the potential protective effect of curcumin against UV radiation-induced , , , , and expression in immortalized keratinocytes (HaCaT), hepatocellular carcinoma (HepG2), and lung adenocarcinoma (A549) cells. Cells were exposed to UV-B radiation for different periods and treated with curcumin at different concentrations to evaluate dose-related trends in DNMT and HDAC gene expression compared with untreated UV-exposed cells. UV exposure increased the DNMT and HDAC gene expression levels in the examined cells dose-dependently. Curcumin exposure resulted in decreased mRNA expression levels of DNMT and HDAC gene expression. In our experimental setup curcumin modulated the transcription of DNMT and HDAC genes in A549 and HaCaT cells in a dose-dependent manner. In HepG2 cells, UV-B induced a less pronounced, but still significant, increase in the examined gene expression levels. This effect was also dose-dependently decreased by curcumin, although less markedly. Future studies are warranted to examine if curcumin combined with other chemopreventive agents through the HDAC and DNMT inhibitory activity at the gene expression level can exert a synergistic effect and may potentially supplement cancer therapeutic strategies. - Source: PubMed
Publication date: 2026/03/17
Zand AfshinRaposa Bence LSzép DávidMacharia John MNowrasteh GhodratollahBudán FerencVarjas Tímea - Glioblastoma (GBM) is characterized by pronounced tumor heterogeneity and a complex immune microenvironment, contributing to poor patient survival outcomes. In this study, we comprehensively dissected the tumor microenvironment (TME) and uncovered potential molecular mechanisms by integrating single-cell, bulk, and spatial transcriptomic data. Hallmarks of malignancy and cell cycle regulatory pathways were consistently enriched across these modalities, promoting tumor cell proliferation and progression. Using machine learning algorithm, we identified seven hallmark-related prognostic signatures (HMsig), namely AEBP1, ASF1A, PRPS1, DCC, OPHN1, IL13RA2, and HDAC5-whose predictive importance was validated through SHAP analysis. Ligand-receptor (LR) interaction analysis further revealed that interactions involving OPHN1 were associated with poorer prognosis. Along the pseudotime trajectory of T-cell differentiation, immune checkpoint genes (ICGs) LAG3, PDCD1, and HAVCR2 were substantially upregulated. Notably, synergistic transcriptional regulation between tumor-related HMsig genes and ICGs in T cells was identified as a key factor influencing patient survival. Spatial transcriptomic analysis demonstrated the existence of synergistic gene interactions, deciphering the immunomodulatory functions of GBM biomarkers within the TME. - Source: PubMed
Publication date: 2026/03/25
Li TengyueMi WanqiYan HuaruiMa YiningJiang HanYang XiaoxuZhang YunpengHu Congxue - Major depression (MD) has been linked to both neuroinflammation and impaired synaptic plasticity. Furthermore, epigenetic mechanisms involving certain histone deacetylases (HDACs) may initiate these changes. Specifically, altered expression of particular HDACs, including HDAC5, HDAC2, SIRT1, and SIRT2, has been associated with depressive-like behavior, suppressed levels of brain-derived neurotrophic factor (BDNF), and the promotion of neuroinflammation. Additionally, changes in these HDACs within peripheral blood mononuclear cells might contribute to peripheral low-grade inflammation. Here, we investigated the influence of MD on the regulation of specific epigenetic targets, alongside the expression of genes involved in neuroplasticity and inflammation. We analyzed fluorescence-activated cell sorting (FACS)-isolated monocytes (classic, intermediate, and non-classic) and T-cells (CD3+) from fifty-six patients with moderate-to-severe MD and age- and sex-matched healthy controls. Decreased HDAC5 cytoplasm/nucleus ratio in MD monocytes were observed. Moreover, decreased HDAC5 cytoplasm/nucleus ratio negatively correlated with illness severity in MD monocyte subsets and T-cells. In addition, decreased SIRT2 cytoplasm/nucleus ratio in monocytes and T-cells were observed. Gene expression studies showed an increase in HDAC5 mRNA both in intermediate monocytes and T-cells as well as an increase of SIRT2 in intermediate monocytes. Moreover, decreased expression of the neuroplasticity biomarker BDNF, known to be regulated by these two epigenetic enzymes was observed in intermediate monocytes and T-cells. Moreover, an increase of ADRB2 mRNA, encoding the β2 adrenoceptor was observed in classic monocytes. Furthermore, in these cells, both ADRB2 and IL-6 mRNA showed a negative correlation with the HDAC5 cytoplasm/nucleus ratio. Importantly, logistic regression analysis revealed that changes observed with ADRB2 in classic monocytes, SIRT2 in intermediate monocytes and HDAC5 in T-cells were associated to MD with a moderate discriminatory accuracy. These studies suggest that MD promotes nuclear enrichment of the epigenetic enzymes HDAC5 and SIRT2 in monocytes and T-cells of MD patients. These epigenetic changes could potentially contribute to the observed adrenergic and neuroplasticity markers alterations in monocytes and T-cells respectively. Further, some of the targets studied were associated to MD with an acceptable diagnostic value, suggesting the need to enlarge the cohort in order to identify whether they are biomarkers for MD. - Source: PubMed
Publication date: 2026/03/06
Cortés-Erice MaríaGarayo-Larrea AinhoaFernández-Ovejero RaquelAubá EnriqueLizaso SandraAldaz PabloBes-Rastrollo MairaGil José LópezBarrado LauraOrtuño FelipeMolero PatricioTordera Rosa M - Histone deacetylases (HDACs), as key epigenetic regulators, serve a central role in tumorigenesis and progression by modulating chromatin architecture and gene transcription. In recent years, notable advances have been made in elucidating the pan-cancer mechanisms of HDACs and their inhibitors (HDACis), as well as in performing clinical studies, with their antitumor activity becoming a major research focus. The present review summarized the classification and molecular mechanisms of HDACs alongside their roles in various malignancies including ovarian cancer, endometrial carcinoma, glioma, osteosarcoma and multiple myeloma. The present review specifically elaborated on the relationship between particular isoforms, such as HDAC3, HDAC5, HDAC7 and HDAC11, and tumor progression, detailing associated signaling pathways. The present review systematically evaluated the current clinical applications of HDACis, examining both monotherapy and combination therapy efficacy alongside existing challenges. Furthermore, the present review discussed recent progress in structural modifications aimed at enhancing selectivity while reducing toxicity, as well as novel targeting strategies. Concluding with perspectives on HDAC-based therapies, the present review underscores the key importance of precision targeting and combinatorial approaches to improve patient outcomes in the future. - Source: PubMed
Publication date: 2026/02/24
Lin RunlingZhang YuLi HongLiang Fan - Both histone acetyltransferases (HATs) and histone deacetylases (HDACs) control the acetylation state of conserved lysine residues in histone tails. Thereby, modulating chromatin structure and gene transcription. Disturbance of this precisely balanced acetylation state contributes to neuronal, cardiovascular, muscle degenerative, autoimmune diseases and cancer. To restore this delicate balance, HDAC inhibitors (HDACi) are employed. However, employing pan-HDAC inhibitors, that target a broad spectrum of HDACs, often leads to significant side effects. Therefore, the development of isoform specific inhibitors is urgently needed. Among the HDAC family, class IIa HDACs, particularly HDAC5, have emerged as promising drug targets due to their tissue-specific expression patterns and presence in large regulatory complexes. Recent progress in selective class IIa HDAC inhibition has led to the development of novel HDACi that contain a 5-(trifluoromethyl)-1,2,4-oxadiazole (TFMO) zinc-binding group (ZBG) to interact with the Zn²⁺ ion in the active site, avoiding the drawbacks associated with promiscuous hydroxamic acid–based HDACi. This study focuses on the in vitro characterization of the catalytic domain of human HDAC5 and its inhibition by the TFMO-based HDACi FFK24 and NT160. Our findings contribute to a better biochemical understanding of the kinetic parameters of HDAC5 activity and support the development of selective inhibitors targeting class IIa HDACs. - Source: PubMed
Publication date: 2026/02/27
Mammen ChristianHornung Fenja MAnzenhofer ChristianSchumacher JuliaReiners JensLi JingyuMazzone FlaminiaBilsing Florestan LKassack Matthias UKurz ThomasSmits Sander H J