Polyclonal HDAC9
- Known as:
- Polyclonal HDAC9
- Catalog number:
- pc-369
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal HDAC9
Related genes to: Polyclonal HDAC9
- 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: Polyclonal HDAC9
Related articles to: Polyclonal HDAC9
- 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 - Vascular calcification (VC), characterized by calcium deposition in arterial walls, is a major risk factor for cardiovascular morbidity and mortality. While genome-wide association studies (GWAS) have identified susceptibility loci for specific vascular beds, such as coronary artery calcification (CAC) and abdominal aortic calcification (AAC), single-phenotype studies may overlook pleiotropic variants. This study aims to elucidate the shared genetic architecture of CAC and AAC and translate these findings into biological insights and potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/15
Li HuibinLi Gaofei - Excessive intake of Titanium dioxide nanoparticles (TiO NPs) in children may lead to abnormal development of cartilage growth plates. Elucidating the mechanism underlying the toxicity of TiO NPs on chondrocytes contributes to the prevention and clinical treatment of short stature in children. Herein, we found that TiO NPs inhibited chondrocyte proliferation and differentiation. Elevated levels of oxidative stress and activation of ferroptosis were observed in TiO NP-exposed chondrocytes. HDAC9 was downregulated in TiO NP-exposed chondrocytes, of which overexpression reversed TiO NP-mediated detrimental effects. Mechanistically, TiO NPs inhibited TDP-43 to impair nucleocytoplasmic translocation and mRNA stability of HDAC9. TDP-43 overexpression protected growth plate chondrocytes from TiO NPs exposure, which were blocked by HDAC9 knockdown. TiO NPs inhibited p53 deacetylation by suppressing nucleocytoplasmic translocation of HDAC9. HDAC9 upregulated BCL6 and strengthened the interaction of BCL6 and Miz-1 to suppress p21 transcription in chondrocytes. The combination of HDAC9 overexpression and Pifithrin-α efficiently abolished TiO NP-mediated detrimental effects in vivo. In conclusion, TiO NPs suppresses p53 deacetylation via inhibiting HDAC9 nucleocytoplasmic translocation to impair chondrocyte proliferation and differentiation through IGF1/mTOR signaling. - Source: PubMed
Publication date: 2026/05/28
Feng LihuaLuo JinghuaChen XiangxiangXia YananXu YunpingLi YangeLiu Yang - Post-stroke depression (PSD) affects approximately 30% of stroke survivors and worsens functional outcomes, yet its biological basis remains poorly understood. - Source: PubMed
Xu Zhi-JieZhang Su-XiangLi Ji-LingWu Jia-JiaMa JieMa Zhen-ZhenTao Ji-MingHua Xu-YunXu Jian-Guang - Intervertebral disc degeneration is a leading cause of chronic low back pain, characterized by cellular senescence, extracellular matrix disintegration, and chronic inflammation. However, the key epigenetic regulators that orchestrate senescence and the resultant inflammatory cascade in disc degeneration remain poorly understood. - Source: PubMed
Publication date: 2026/05/18
Cheng XingdongWang JingjingChen YuqingXue RongGao Zengxin