Ask about this productRelated genes to: HDAC4 antibody
- 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 antibody
Related articles to: HDAC4 antibody
- Spinal Muscular Atrophy (SMA) is a neuromuscular disorder associated with motor neuron degeneration, yet the role of the well-conserved Survival of Motor Neuron (SMN) protein in muscle remains insufficiently understood. Using the Drosophila neuromuscular junction (NMJ) as a model, we combined tissue-specific Smn depletion with transcriptomic profiling and prior genetic modifier screens to identify SMN-dependent genes that contribute to synaptic architecture. Functional screening of candidate genes significantly and selectively effected in muscle identified genes whose knockdown phenocopied NMJ morphometry defects characteristic of Smn loss-of-function (LOF), including FER, CAP, HDAC4, Nhe2, and Raskol. Unlike other genes in this group, analysis of postsynaptic architecture using a subsynaptic reticulum (SSR) biomarker disrupted by Smn LOF singled out the conserved tyrosine kinase FER as an SMN-dependent gene in muscle that influences this prominent feature of the NMJ. Analysis of different FER transcripts suggests that elevation of the FERp100 protein isoform in Smn LOF muscle tissue leads to a dominant-negative effect likely to disrupt signaling via the MAPK-family kinase Basket (Bsk) to regulate the downstream phosphatase Puckered (Puc). - Source: PubMed
Yokokura TakakazuHeggeness HansineYoshikawa SeikoAlaimo SalvatoreBoonrawd ThiradaAhluwalia NavpreetVan Dihn Thi ThuFerro AlfredoMcNeill Elizabeth MVan Vactor David - The malignant progression of nonsmall cell lung cancer (NSCLC) is closely related to cancer stemness. Histone deacetylase 4 (HDAC4) plays a regulatory role in lung cancer, but its effect on NSCLC stemness remains unclear. This study aimed to investigate the role and mechanism of HDAC4 in NSCLC stemness. - Source: PubMed
Chen ChangxianJiang XiaomingYao ZhenwuSun JiaxueZhang LijuXu MingyuBao WeiminLiu Weijun - Uveal melanoma (UM) is a rare but aggressive cancer arising from cells of the uveal tract that is highly resistant to therapy once it has metastasized. In drug screening experiments, we identified a high sensitivity of primary UM cell lines to the pan-histone deacetylase (HDAC) inhibitor panobinostat and addressed the question whether two class IIa HDACs, HDAC4 and HDAC5, could serve as potential therapeutic targets in UM. Selective pharmacological inhibition of HDAC4/5, as well as stable knockdown of HDAC4 or HDAC5, did not strongly affect cell viability, differentiation, apoptosis or necrosis, and did not sensitize cells to other HDAC or MEK inhibitors. Proteogenomics analysis revealed 73% concordance and only 7% discordance in the expression of transcripts and proteins. Concordance reached 92% for significant transcripts. Despite the lack of severe global gene and protein expression changes in HDAC4- or HDAC5-knockdown UM cell lines, the expression of individual cancer-related genes and signaling pathways was differently regulated following HDAC4 or HDAC5 knockdown. This was particularly evident in the NF-κB pathway, which showed decreased NF-κB p65 phosphorylation in UM cell lines with monosomy in chromosome 3 (M3) genotype and mutations in BRCA1-associated protein 1 (BAP1). In summary, our results suggest that HDAC4/5 inhibitors alone are insufficient for monotherapy in UM cells, but the identification of HDAC4/5-regulated genes involved in cancer progression provides a rationale for exploring combination strategies that include HDAC4/5 inhibition. - Source: PubMed
Publication date: 2026/09/22
Henning SvenjaKutzner Tanja JSchneider MartinGonzález-Gimeno TeresaZheng YueBerchner-Pfannschmidt UttaHelm DominicGiebel BerndBechrakis Nikolaos EPeña-Llopis Samuel - Sixty novel 5-(trifluoromethyl)-1,2,4-oxadiazole derivatives were designed by scaffold hopping from the diamide lead 6n and synthesized to examine ether, thioether, and sulfoxide linkers. Greenhouse assays against Phakopsora pachyrhizi identified FM-12818 (B5) as a leading thioether derivative, with an EC50 of 0.45 mg·L-1, comparable to flufenoxadiazam (0.49 mg·L-1). FM-12818 also provided 80% control of Puccinia triticina at 0.391 mg·L-1 under the tested conditions. Docking to a human HDAC4 surrogate and DFT calculations suggested a putative zinc-binding orientation and linker-dependent electronic differences, including a possible π-sulfur contact. These computational observations generate hypotheses for the structure-activity relationship but do not establish HDAC inhibition or a distinct mode of action. FM-12818, therefore, represents a potent greenhouse lead for further target validation, field efficacy, and safety studies. - Source: PubMed
Liu YuandongYe JialinHuang YuxinZhang JingZhang Lixin - Myostatin (MSTN), encoded by the MSTN gene, is a critical negative regulator of skeletal muscle mass. This study aims to identify and characterize the miRNAs involved in the development of the double-muscling phenotype in MSTN-deficient rabbits. We performed high-throughput sequencing to analyze the miRNA expression profiles in gluteus maximus tissue from wild type (MSTN) and MSTN-KO (MSTN and MSTN inclusive) rabbits. Differentially expressed miRNAs (DEmiRNAs) were identified, and their potential target genes were predicted. Functional enrichment analysis of these target mRNAs was conducted using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database to elucidate the involved biological pathways and regulatory networks. A total of 25 DEmiRNAs (13 downregulated and 12 upregulated, |logFC| ≥ 1.0, adjusted p < 0.05) and 1178 differentially expressed mRNAs (408 upregulated and 770 downregulated, |logFC| ≥ 2.0, adjusted p < 0.05) were identified in MSTN-KO compared to MSTN rabbits. Bioinformatics analysis revealed that the target genes of these DEmiRNAs were significantly enriched in key pathways governing muscle growth and metabolism, including the PI3K-Akt signaling pathway, MAPK signaling pathway, and pathways related to ECM-receptor interaction and insulin signaling. Notably, many predicted target mRNAs are expressed by genes that encode key inhibitors of myogenesis (e.g., HDAC4) and major extracellular matrix components (e.g., COL4A3, POSTN). Our results demonstrate that MSTN deficiency induces a distinct and widespread change in the miRNA expression landscape of skeletal muscle. - Source: PubMed
Song Zhi-XianKyaw Paing OoFarhab MuhammadZhang TingLiang JingyanYuan Yu-Guo