Ask about this productRelated genes to: HDAC3 antibody
- 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 antibody
Related articles to: HDAC3 antibody
- Autoantibodies (AABs) are valuable biomarkers for diagnosing and monitoring autoimmune diseases and cancer. Conventional AAB profiling methods, such as enzyme-linked immunosorbent assay and immunoblot, are time-consuming, labor-intensive, and limited in multiplexing capacity. Luminex xMAP technology overcomes these limitations by enabling high-throughput, multiplexed AAB detection via bead-based immunoassays. However, the random immobilization of antigens on Luminex beads can lead to suboptimal epitope exposure, reduced binding sensitivity, and inconsistent assay performance. This study examines whether oriented antigen immobilization via genetic code expansion and click chemistry enhances binding sensitivity on the Luminex platform compared to random immobilization via conventional amine coupling. We selected three human antigenic proteins, HDAC3, RPS17, and RPS4Y1, and incorporated the noncanonical amino acid (ncAA) -((2-azidoethoxy)-carbonyl)-l-lysine (AzK) at a genetically defined position using the stop codon suppression method. This enabled site-specific conjugation of the antigens to dibenzocyclooctyne (DBCO)-functionalized beads via strain-promoted azide-alkyne cycloaddition (SPAAC). Binding sensitivity was assessed using serum samples from 88 individuals (22 healthy and 66 lung carcinoma patients). Oriented immobilization of RPS4Y1 AzK on DBCO-beads resulted in a 2.5-fold increase in binding sensitivity compared to random immobilization on COOH-beads, demonstrating that controlled antigen orientation improves epitope accessibility and enhances AAB detection sensitivity. These findings establish site-specific antigen immobilization via genetic code expansion and click chemistry as a superior alternative to conventional amine coupling. This immobilization approach significantly improves AAB detection and holds broad potential for applications such as antibody profiling, diagnostics, and drug screening on the Luminex and other biosensing and diagnostics platforms, where high sensitivity and accuracy are essential. - Source: PubMed
Publication date: 2026/04/10
Kolanovic DajanaHofner ManuelaHuber JasminWeinhaeusel AndreasWiltschi Birgit - A main mechanism of β-cell dysfunction in diabetes is loss of identity, controlled by transcription factors that induce identity gene expression and disallowed gene repression. How transcription factors facilitate simultaneous expression and repression is not fully understood, representing a knowledge gap in diabetes research. We identify the transcriptional co-factors transducin β-like 1 x-linked (TBL1X) and its homolog TBL1X-related (TBL1XR1, together TBL/R1) as crucial regulators of β-cell identity and determinants of diabetes development and progression. β-cell specific TBL/R1 knockout in mice leads to progressive hypoinsulinemia and hyperglycemia. scRNA-sequencing reveals loss of β-cells, emergence of polyhormonal cells, and reduced β-cell maturity upon TBL/R1 knockout. Interactome screens and chromatin immunoprecipitation show TBL/R1 directly regulate insulin promoter activity through a PAX6-HDAC3 gene regulatory network, evident also in human models. TBL/R1 associates with diabetes in humans, thus our study uncovers an additional regulatory layer maintaining β-cell identity crucial for diabetes development and progression. - Source: PubMed
Publication date: 2026/04/23
Walth-Hummel Alina AJouffe CelineWeber PeterMotzler KarstenGeppert JuliaSterr MichaelGan WeiSzczerbinska IwonaKönig Ann-ChristineHauck Stefanie MTerron-Exposito RaulHass DanielaWang CongcongDyar Kenneth ALyon James GLickert HeikoÄmmälä CarinaHerzig StephanAshcroft Frances MBakhti MostafaMacDonald Patrick ERohm Maria - Ischemia-induced retinopathy is a defining feature of prevalent ocular conditions, including diabetic retinopathy and central retinal artery or vein occlusion. Therapeutic interventions for ischemic retinopathies show limited efficacy and adverse effects, highlighting the need to thoroughly investigate the underlying mechanisms. Histone deacetylase 3 (HDAC3), a member of the histone deacetylase family, plays a central role in regulating gene expression in myeloid cells (microglia and macrophages). We recently showed that myeloid HDAC3 deletion promotes tissue repair and functional recovery after retinal ischemia-reperfusion (IR) injury via efferocytosis, a process by which myeloid cells engulf and clear apoptotic cells. Here, we investigated the mechanism by which myeloid HDAC3 deletion enhances efferocytosis. Employing an in vitro efferocytosis assay coupled with RNA sequencing on HDAC3 KO macrophages revealed that the secreted protein, CD5 molecule-like (CD5L), was the most upregulated among other pro-efferocytic genes. In vivo, we found that CD5L levels markedly increased in the retinas of myeloid HDAC3 KO mice subjected to IR injury, and its expression colocalized with myeloid cells. Co-immunoprecipitation experiments showed that HDAC3 represses CD5L expression in a liver X receptor (LXRα)-dependent manner. Additionally, we found that CD36, a receptor for CD5L that facilitates the clearance of apoptotic cells, was upregulated in retinal myeloid cells after IR. In vitro, CD5L treatment enhanced efferocytosis via CD36. We then evaluated the role of CD5L in retinal IR injury using in vivo neuronal, vascular, structural, and functional endpoints. CD5L KO mice showed worsened outcomes after IR, whereas treatment with recombinant CD5L was protective against retinal ischemic injury. Collectively, our findings suggest that deleting HDAC3 enhances macrophage efferocytosis by upregulating the CD5L/CD36 axis. CD5L may serve as a promising therapeutic target to improve outcomes in ischemic retinopathy. - Source: PubMed
Publication date: 2026/04/20
Shahror Rami AZaman BushraChuesiang PiyananWild MelissaShosha EsraaLeung Yuet-KinMu ShengyuRusch Nancy JFouda Abdelrahman Y - Diffuse large B-cell lymphoma (DLBCL) refers to an aggressive lymphoma that arises from germinal center (GC) B cells, which differentiate into plasma cells to produce high-affinity antibodies. A total of 40% of patients with DLBCL relapse or are refractory to the conventional immunochemotherapy treatment, usually with fatal consequences. DLBCL is characterized by profound alterations in the epigenome, which is correlated with poor survival. The abnormal epigenetic landscape of DLBCL tumors is associated with a blockade in GC exit and differentiation programs, which are regulated by the transcription factor BCL6. This aberrant repression of BCL6 target genes is mediated by (1) increased DNA methylation and (2) the loss of acetylation of lysine 27 of histone 3 through the recruitment of histone deacetylase 3 (HDAC3). Therefore, we investigated the efficacy of the hypomethylating agent 5-azacitidine (5-aza) and a specific HDAC3 inhibitor (HDAC3i) against DLBCL. We found that the treatment of activated B cell-like and GC B cell-like DLBCL cells with 5-aza plus HDAC3i had a potent synergistic antitumor activity in vitro and in vivo, which was superior to the effect of each single drug or 5-aza combined with nonspecific HDACi and, importantly, was not associated with toxicity in normal T cells. We also demonstrated that, compared with that with each drug used as single agents, the combined 5-aza and HDAC3i treatment induced the epigenetic remodeling of DLBCL cells, which resulted in a more potent reexpression of differentiation genes, including and . Our results highlight the importance of specifically targeting multiple layers of the epigenome to maximize the efficacy of epigenetic-based therapies. - Source: PubMed
Publication date: 2026/03/02
Calaud CalixteSerrano-Lopez Emilio MCluse Leonie ATodorovski IzabelaMardivirin ThomasTeater Matt RMaarad AbdelillahTawfic NouraFraser Peter JGuiraud KillianDupont CoralieMenigot CorinneSant'Anna-Silva Ana Carolina BYoannidis DavidSemple TimKerreneur EmelineRocchi StéphaneJacquel ArnaudMelnick Ari MJohnstone Ricky WDominguez Pilar M - Biological sex regulates fundamental neurobiology, as well as the etiology and prevalence of neuropsychiatric disorders. Cyclin-dependent kinase 5 (Cdk5) is a neuronally enriched kinase that regulates synaptic plasticity, neuronal homeostasis, and hippocampal-dependent memory. While Cdk5 protein activity is necessary and sufficient to promote memory in male rodents, its role in females and its gene regulation in either sex remain poorly understood. In males, Cdk5 protein inhibition impairs fear memory. We previously showed that fear conditioning activates gene expression and increases permissive chromatin acetylation in male, but not female hippocampus. We hypothesize that gene repression would impair fear memory in males. We developed an excitatory neuron-specific, CRISPR/dCas9-HDAC3 epigenetic editing tool to target histone acetylation at the endogenous Cdk5 promoter. This strategy reduced histone acetylation and decreased Cdk5 mRNA, protein, and kinase activity in both sexes. Interestingly, repression in hippocampal neurons impaired fear and spatial memory in both male and female mice. Targeted deacetylation also evicted the transcription factor CREB1 from the Cdk5 promoter, revealing a link between histone acetylation and Cdk5 transcriptional activation. These findings demonstrate that acetylation in neurons is necessary for hippocampal memory in both sexes, providing new insight into sex-specific epigenetic regulation of memory. - Source: PubMed
Publication date: 2026/04/10
Rodríguez-Acevedo Kiara LWinter Julia JAlvarez Megan ISase AjinkyaCzarnecki KyleHeller Elizabeth A