Polyclonal HDAC4
- Known as:
- Polyclonal HDAC4
- Catalog number:
- pc-364
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal HDAC4
Related genes to: Polyclonal HDAC4
- 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: Polyclonal HDAC4
Related articles to: Polyclonal HDAC4
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies, and elevated HDAC activity contributes to tumor progression and drug resistance. In the current study, we designed and synthesised a new series of piperazine-linked 1H-1,2,3-triazole derivatives (6a-6f, 7a-7f, and 8a-8f) and evaluated their antiproliferative activities in human breast cancer cells. All synthesised compounds were characterized using H NMR, C NMR, F NMR, and high-resolution mass spectrometry (HRMS-ESI + -MS) to confirm their structures. The compound 7e exhibited potent growth inhibition in MDA-MB-231 cells with an IC₅₀ of 27.59 μM, while showing low toxicity toward HUVEC cells. Cell-cycle analysis revealed significant accumulation of cells in the G2/M phase. Mechanistically, compound 7e significantly decreased HDAC activity (63% compared to control) at 30 μM, and induced mitochondrial dysfunction as evidenced by a marked loss of ΔΨm. Furthermore, Molecular docking across selected HDAC isoforms indicated that 7e can adopt favorable binding poses within conserved HDAC catalytic pockets; HDAC2 showed the best Glide XP docking score, whereas MM-GBSA refinement predicted a more favorable binding free energy for HDAC4. Collectively, these results identify this piperazine-triazole scaffold as a promising lead for TNBC therapy and support further structural optimization and preclinical investigation. - Source: PubMed
Publication date: 2026/06/18
Moghtaderi HassanKhan Sadiq NoorKamangar MohammadNosood Yazdanbakhsh LotfiAlhinai AbdulrahmanRahman Shaikh MizanoorCsuk RenéAvula Satya KumarAl-Harrasi Ahmed - Hypoxia-inducible factor-2α (HIF-2α) is a key regulator of cellular adaptation to hypoxia, but its role in osteoarthritis (OA) remains incompletely defined. This study aimed to investigate the contribution of HIF-2α to OA pathogenesis and the underlying molecular mechanisms. Human cartilage specimens were collected to examine HIF-2α expression and components of the histone deacetylase 4 (HDAC4) signaling pathway using Western blotting, quantitative real-time PCR, and immunohistochemistry. An in vitro OA model was established in chondrocytes using interleukin-1β (IL-1β), followed by HIF-2α knockdown with small interfering RNA and overexpression via adenoviral transduction. Chondrocyte apoptosis was assessed by flow cytometry and TUNEL staining. To evaluate in vivo effects, HIF-2α was silenced using an adeno-associated viral vector in a rat OA model induced by anterior cruciate ligament transection (ACLT). Disease progression was assessed by X-ray, computed tomography (CT), FMT® small animal in vivo fluorescence molecular tomography imaging system, Safranin O staining, and immunohistochemistry. HIF-2α expression was significantly increased in cartilage from OA patients and ACLT rats. In vitro, HIF-2α modulation altered HDAC4 expression and downstream apoptotic signaling. Knockdown of HIF-2α reduced chondrocyte apoptosis and attenuated cartilage degeneration in vivo. These findings indicate that HIF-2α promotes OA progression by regulating chondrocyte apoptosis and matrix homeostasis through the HDAC4-ATF4-CHOP pathway. This study identifies a previously unrecognized mechanism linking HIF-2α to OA and highlights its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/06/18
Jiang PinpinWang HangLi YujiaZhang YuanyuHuang JingruiXu YukunRong DahaiRuan DanniWang YaoYuan JieLi Pengcui - Transforming growth factor-beta1 (TGF-β1) regulates bone formation through Runx2, a bone transcription factor, and Runx2 activity is regulated by several coactivators and corepressors. Histone deacetylase 4 (HDAC4) functions as a transcriptional corepressor, and it downregulates Runx2 activity in osteoblastic cells. Emerging evidence suggests that non-coding RNAs, particularly microRNAs (miRNAs), significantly influence normal and abnormal bone homeostasis. In this study, we identified miR-3064-3p, which targets HDAC4 in osteoblasts. Our findings demonstrated that TGF-β1 upregulates miR-3064-3p, which in turn downregulates HDAC4, leading to increased acetylation of Runx2 in osteoblastic cells. Conversely, inhibition of miR-3064-3p restored HDAC4 levels and reduced Runx2 acetylation. Inhibition of miR-3064-3p also decreased the expression of osteogenic transcription factors in differentiating osteoblasts. miR-3064-3p directly targeted the 3' untranslated region of HDAC4 in osteoblasts. In vivo analyses using a rat femoral defect model demonstrated that TGF-β1 significantly enhances bone regeneration, and the miR-3064-3p inhibitor markedly impaired this regenerative process, indicating its essential role in mediating TGF-β1-driven bone regeneration. Collectively, these findings highlight the pivotal role of the TGF-β1/miR-3064-3p/HDAC4/Runx2 axis as a positive regulator of bone formation. - Source: PubMed
Publication date: 2026/06/17
Saranya IyyappanPreetha DilipkumarNivruthi SasiSelvamurugan Nagarajan - Craniofacial large bone defects possess limited self-repair capacity. This study identifies histone deacetylase 4 (HDAC4) as a key epigenetic repressor of osteogenesis in human adipose-derived stem cells. Inhibiting HDAC4, either genetically or pharmacologically with tasquinimod, enhanced histone acetylation and activates SMAD4 expression, thereby promoting bone formation. A sustained-release hydrogel delivering tasquinimod was developed and demonstrated to significantly enhance bone regeneration in critical-sized cranial and mandibular defects in mice. The findings reveal a promising localized epigenetic strategy for repairing craniofacial bone defects. - Source: PubMed
Publication date: 2026/06/11
Yu LiyuanXia KaiWang YijueHu ZhiaiLiu JunZou ShujuanChen Jianwei - Pathological cardiac hypertrophy is a major precursor to heart failure, yet the transcriptional mechanisms that restrain maladaptive remodeling remain incompletely defined. Class IIa histone deacetylases (HDAC4, HDAC5, and HDAC9) modulate cardiac hypertrophy but exhibit paradoxical effects, underscoring the need for more precise therapeutic targets. Unlike other Class IIa HDACs, HDAC7 is not expressed in adult cardiomyocytes (CMs), and its role in cardiac stress responses is unknown. - Source: PubMed
Publication date: 2026/06/05
Bu JinHand Sophie MGuo ShuliangJang JihyunLi Deqiang