HDAC2 antibody - middle region (ARP32619_P050)
- Known as:
- HDAC2 (anti-) - middle region (ARP32619_P050)
- Catalog number:
- arp32619_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HDAC2 antibody - middle region (ARP32619_P050)
Related genes to: HDAC2 antibody - middle region (ARP32619_P050)
- Gene:
- HDAC2 NIH gene
- Name:
- histone deacetylase 2
- Previous symbol:
- -
- Synonyms:
- RPD3, YAF1, KDAC2
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2019-02-19
Related products to: HDAC2 antibody - middle region (ARP32619_P050)
Related articles to: HDAC2 antibody - middle region (ARP32619_P050)
- Diabetic painful neuropathy (DPN) is a common complication of diabetes. Despite ongoing efforts, the underlying biological mechanisms of DPN remain poorly understood. Hyperglycemia-mediated oxidative stress can affect cell barrier properties, triggering low-grade inflammation. Previous studies have reported increased histone deacetylase (HDAC) activity and altered expression of tight junction proteins in diabetes, which may link to nerve damage. This study examined the effects of the HDAC inhibitor FK228 on cell barrier-mediated changes in the spinal cord and dorsal root ganglia (DRG) of type 2 diabetic mice. Diabetic mice were treated with FK228 (1 mg/kg, twice a week for 3 weeks). Behavioral assessment of cold hypersensitivity was assessed at the end of the treatment regimen. In vitro studies were conducted using ND7/23 immortalized DRG cells. The expression of tight junction proteins (occludin, claudin-1, and zona occludens-1 or ZO-1) and a number of stress-related cellular markers, including HDAC2, growth-associated protein (GAP) 43, epidermal growth factor receptor (EGFR), and nuclear factor erythroid 2-related factor (Nrf2), were evaluated in DRG, spinal cord tissue, and cultured ND7/23 DRG cells following treatment. FK228 treatment demonstrated changes in cold pain sensitivity as well as the expression of tight junction proteins and stress related markers in both in vivo and in vitro models of diabetic neuropathy. These findings indicate that HDAC inhibition by FK228 may support the maintenance of tight junction protein expression and alter cellular stress responses in the spinal cord and DRG, suggesting a possible role of FK228 in mitigating DPN. - Source: PubMed
Publication date: 2026/07/31
Chen EileenThakur VikramChowdhury ErinaMisra AmoghValdez CarlosChattopadhyay Munmun - Histone deacetylases (HDACs) act as transcriptional repressors and play essential roles in mammalian development. However, data on the expression and subcellular localization of HDACs in the tongue and oral mucosa remain limited. This study aimed to investigate the spatiotemporal expression patterns of HDACs in the mouse tongue and oral mucosa during postnatal development and aging. - Source: PubMed
Publication date: 2026/08/13
Yang ChuboWang JingruWang MingxingLi HuishuKong JiaqiGuo XinruZhan Yuanbo - TRIM28, a member of the tripartite motif (TRIM) family, functions as a transcriptional coregulator involved in maintaining genome stability during mitosis. However, transcriptional activity is barely detectable during oocyte meiotic maturation. In this study, we explored the role of TRIM28 in mouse oocytes and found that it was constitutively expressed in the early stages of oocyte meiotic maturation, with predominant nuclear localization in germinal vesicle (GV)-stage oocytes. TRIM28 depletion caused defective germinal vesicle breakdown (GVBD), but oocytes that successfully underwent GVBD displayed unimpaired first polar body (PB1) extrusion. TRIM28 depletion impaired CDK1 activity and reduced cyclin B1 levels, leading to a delay in the G2/M transition. This delay may be attributed to altered levels of HDAC2-mediated H4K12ac and H3K4me2-modulated H3K9me2 in nonsurrounded nucleolus (NSN)-type GV oocytes, which decreased transcription activity. Additionally, TRIM28-depleted oocytes exhibited elevated γ-H2A.X expression, accompanied by aberrant expression of CHK1 and CHK2, as well as dysregulated expression of RAD51, which were collectively contributed to GVBD failure in mouse oocytes. In conclusion, our findings indicate that TRIM28 participates in the regulation of the G2/M transition during mouse oocyte meiotic maturation, acting through the modulation of histone modifications and DNA damage repair. - Source: PubMed
Publication date: 2026/08/10
Ma Rui-JieTang Meng-MengLu Ping-ShuangZhang Hao-LinJu Jia-QianWang Ya-PingZhang Kun-HuanWang YueSun Shao-Chen - Gut dysbiosis contributes to irritable bowel syndrome (IBS) pathogenesis and fungi exert independent effects on IBS patients, independent of bacterial influence. IBS patients exhibit elevated fecal Candida levels but the specific role of Candida in IBS remains unclear. - Source: PubMed
Publication date: 2026/08/09
Liu AoAi YanYang PengchengZhang LiHong GaichaoSchnabl BerndXu KeshuCai KailinHou XiaohuaChu Huikuan - RhoA-a member of the Rho family of GTPases-critically regulates synaptic plasticity and immune cell function, which have emerged as key mechanisms in schizophrenia pathogenesis. - Source: PubMed
Publication date: 2026/08/08
Khaki MahsaDavoodian Nahid