HDAC5, His, Human
- Known as:
- HDAC5, histidine, Human
- Catalog number:
- Z03083-50
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- HDAC5 His Human
Related genes to: HDAC5, His, Human
- Gene:
- HDAC5 NIH gene
- Name:
- histone deacetylase 5
- Previous symbol:
- -
- Synonyms:
- KIAA0600, NY-CO-9, FLJ90614
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2016-10-06
Related products to: HDAC5, His, Human
Related articles to: HDAC5, His, Human
- 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 - Salt-Inducible Kinase 3 (SIK3) has emerged as a key regulator of peripheral metabolism, however its cellular and molecular function in regulating body weight and energy metabolism, particularly in hypothalamic neurons, remains unclear and largely unexplored. Here, we demonstrate that SIK3 expression is elevated in the hypothalamus of obese mice. Inactivation of SIK3 specifically in orexigenic NPY neurons reduces food intake, increases energy expenditure, and enhances white adipose tissue browning, resulting in resistance to high-fat diet-induced obesity in mice. Pharmacological inhibition of SIK3 with the inhibitor GLPG3970 in diet-induced obese mice led to significant reductions in body weight and adiposity, primarily due to decreased energy intake, with notable improvements in metabolic health. These effects are linked to enhanced central leptin and insulin signaling, and the dephosphorylation and nuclear translocation of key transcriptional metabolic regulators, CRTC1 and HDAC5. These findings reveal a previously unidentified SIK3-mediated pathway that promotes positive energy balance and suggests SIK3 inhibition may offer therapeutic potential for treating obesity and metabolic disorders. - Source: PubMed
Publication date: 2026/06/02
Onda Danise AnnYang Chieh-HsinGoldsmith CallenBeddows Cait ATeo Rui QiZhang LeiYuan XiaoZhuoZhu YifeiLee Man KsOvens Ashley JYu DingyiSakamoto KeiScott John WMurphy Andrew JTsumaki NoriyukiHerzog HerbertDodd Garron TLoh Kim - : Histone deacetylase inhibitors (HDACi) represent a novel class of antineoplastic agents, yet their comprehensive safety profile warrants further investigation. This study aimed to examine the safety of HDACi using the FDA Adverse Event Reporting System (FAERS) and to explore causal relationships through Mendelian randomization (MR) analysis of drug targets. : Adverse drug event (ADE) reports for Vorinostat, Romidepsin, Belinostat, and Panobinostat submitted to the FAERS from their respective market entry dates through 31 December 2023, were analyzed using disproportionality analyses with four algorithms, supplemented by time-to-onset analysis, logistic regression, and MR analysis. : A total of 1360, 1065, 225, and 1234 ADE reports were documented for Vorinostat, Romidepsin, Belinostat, and Panobinostat, respectively. Eight preferred terms, including decreased white blood cell, platelet, and neutrophil counts, hypophosphatemia, hypocalcemia, QT prolongation, increased aspartate aminotransferase, and anemia, exhibited positive signals across all four HDACi. A temporal decline in the risk of most HDACi-related ADEs was observed, and age, gender, and weight were identified as potential confounding factors for important medical events. Notably, MR analysis revealed a positive correlation between HDAC5 expression and serum phosphate levels. : This pharmacovigilance study provides hypothesis-generating evidence that hypophosphatemia may represent a potential class effect of HDACi. - Source: PubMed
Publication date: 2026/04/28
Zhao RuiqiZhang BeiHan MengyaoLv MinlingSun JialingZhou Xiaozhou - Microglia's role in epilepsy through neuroimmune communication is poorly understood. Mechanisms by which neurons activate microglia and how microglia affect neuronal activity to drive seizure-related inflammation remain unclear. Here, we elucidated a crucial axis connecting pathological adenosine triphosphate (ATP) release induced by epileptiform neuronal activity to microglial MEF2A-dependent hyperactivation, which exacerbates epilepsy pathology. In epilepsy models, seizures cause excessive ATP release, activating microglial P2X7 receptors, causing CAMKII phosphorylation. This triggers HDAC5 translocation, freeing MEF2A for acetylation, and enhancing transcription. Acetylated MEF2A increases CD74 and NEK7 expressions, enhancing NLRP3 inflammasome activation and microglial hyperactivation, worsening neuronal hyperexcitability by increasing inhibitory synapses clearance. Targeting microglial MEF2A with parecoxib or AAV knockdown reduced seizure severity and cognitive deficits and maintained synaptic inhibition by reducing excessive microglial phagocytosis. This reveals an ATP-P2X7-Ca⁺- MEF2A signaling axis connecting neuronal injury with pathogenic microglial activation, suggesting MEF2A as a therapeutic target for microglial-neuronal homeostasis restoration in epilepsy pathology. - Source: PubMed
Publication date: 2026/05/22
Wu JinghengFu JiayuanyuanWang ShuaiWu YuzhangWang XuFeng ShangangShi QiWang YuhaoShi YetongFang YehongLan YuWu QiaoliDu ChuanYin ShaoyaXu LixiaYan Hua - This study explores the molecular mechanism of HDAC5 in ferroptosis of intestinal epithelial cells in sepsis-induced acute intestinal injury. - Source: PubMed
Publication date: 2026/05/19
Zhu Jin-PengSun Mei-NaLiu Shi-HuiDu Zhi-An