HDAC7A (Phospho-Ser155) Antibody
- Known as:
- HDAC7A (Phospho-Ser155) Antibody
- Catalog number:
- 11823
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- HDAC7A (Phospho-Ser155) Antibody
Related genes to: HDAC7A (Phospho-Ser155) Antibody
- Gene:
- HDAC7 NIH gene
- Name:
- histone deacetylase 7
- Previous symbol:
- HDAC7A
- Synonyms:
- DKFZP586J0917
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-13
- Date modifiied:
- 2016-10-05
Related products to: HDAC7A (Phospho-Ser155) Antibody
Related articles to: HDAC7A (Phospho-Ser155) Antibody
- 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 - Astrocytes undergo reactive transformations in response to pathological stimuli and play a critical role in neuronal loss associated with Alzheimer's disease (AD). However, the intrinsic mechanisms through which astrocytes detect amyloid-β (Aβ) pathology and develop neurotoxic properties remain inadequately understood. The dysregulation of class IIa Histone deacetylases (HDACs) has been implicated in astrocyte dysfunction under pathological conditions. This study aims to elucidate the role of HDAC7 as an astrocytic mediator of Aβ that drives the formation of neurotoxic reactive astrocytes, and to propose HDAC7 as a potential therapeutic target for mitigating neuronal loss and cognitive deficits in AD. - Source: PubMed
Publication date: 2026/06/22
Ye JinwangDeng YunsongZhang BinggeLi ChengjiaGuo XingYue RuizhuWan HualiHao YueXiao Shifeng - Histone deacetylase 7 (HDAC7), a classical HDAC family member, promotes LPS-inducible glycolysis and inflammatory mediator production in macrophages, innate immune cells that contribute to pathology in metabolic diseases. Here, we investigated myeloid HDAC7 functions in obesity-driven metabolic disease. - Source: PubMed
Publication date: 2026/05/29
Wang YizhuoRamnath DivyaDas Gupta KaustavPrakrithi PBisht KavitaMiller Gregory CXiong ZheruiWan YujunTejo Ellen NCurson James EbAbrol RishikaKeshvari SaharGunther Kimberley SAtkinson Jordan DLoh ZhixuanEngel Jessica AEngwerda Christian RBurgener Sabrina SofiaSchroder KateFairlie David PClouston Andrew DPowell Elizabeth EIrvine Katharine MSullivan Mitchell ALévesque Jean-PierreNguyen QuanSweet Matthew JKarunakaran Denuja - 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 - Class II histone deacetylases (HDAC) orchestrate T cell-dependent immune responses via the epigenetic control of genes and via the post-translational modification of cytoplasmic and nuclear proteins. However, the contribution of single HDAC family members to the differentiation and function of peripheral CD8 T cells remains elusive. We here demonstrate that HDAC7-deficiency leads to the upregulation of immune checkpoint molecules, increased apoptosis and disturbed glutamine homeostasis of peripheral murine CD8 T cells, which we could link to a MEF2D-dependent induction of FasL expression ultimately deterring the survival of HDAC7-deficient CD8 T cells. Likewise, we observed in mouse models of lymphoma, that mice with a T cell-specific deletion of harbor impaired anti-tumor immune responses in syngeneic transfer models of lymphoma and we found that HDAC7 is required for CD8 T cell-dependent memory recall responses in models of lymphocytic choriomeningitis virus infection. Taken together, we identify HDAC7 as a central regulator of cellular exhaustion and apoptosis of peripheral CD8 T cells, controlling CD8 T cell dependent anti-tumor and anti-viral immunity in mice. - Source: PubMed
Publication date: 2026/05/12
Yerinde CansuKeye JacquelineHsiao Hsiang-JungDurlanik SibelFreise InkaNowak FranziskaLetizia MarilenaSchlickeiser StephanObermayer BenediktHuck AdrianFriedrich MarieWu HaoKunkel DésiréeKühl Anja ABauer SebastianThiel AndreasHegazy Ahmed NSiegmund BrittaGlauben RainerWeidinger Carl