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
- Epidermal growth factor receptor (EGFR) "membrane-cytoplasmic-nuclear translocation" occurs in EGFR-19del lung adenocarcinoma (LUAD) following resistance to tyrosine kinase inhibitors (TKIs). This study aimed to elucidate the mechanism of TKI resistance conferred by nuclear EGFR-19del. - Source: PubMed
Publication date: 2026/04/08
Feng YuhengWang MinghaoLiu YangWu XinhaoLin XuyongHan QiangRong Xuezhu - Low vitamin D levels during pregnancy are associated with an increased risk of Gestational Diabetes Mellitus (GDM), potentially mediated by altered vitamin D metabolism. Cytochrome P450 family 24 subfamily A member 1 (CYP24A1) plays a key role in vitamin D catabolism, but its epigenetic regulation in GDM remains unclear. - Source: PubMed
Publication date: 2026/05/06
Milan K LAnuradha MRamkumar K M - Perioperative neurocognitive disorders (PND) are common complications in elderly surgical patients, yet the molecular mechanisms underlying this condition remain poorly understood. Accumulating evidence suggests that HDAC7-a member of the class IIa histone deacetylase (HDAC) family-plays a crucial role in brain injury and can activate the NF-κB pathway independently of its deacetylase activity. In the present study, we investigated whether upregulation of hippocampal HDAC7 contributes to PND through NF-κB-mediated mitochondrial dysfunction and ferroptosis. A tibial fracture model was established in 18-month-old mice, and elevated levels of HDAC7 and phosphorylated NF-κB (P-NF-κB) were detected in the hippocampal CA3 region 3 days after surgery. Moreover, bilateral injections of HDAC7 AAV-shRNA into the CA3 region reduced P-NF-κB levels and alleviated mitochondrial damage. HDAC7 knockdown restored mitofusin 2 (MFN2) expression, reversed the upregulation of acyl-CoA synthetase long-chain family member 4 (ACSL4) and the loss of glutathione peroxidase 4 (GPX4), normalized the levels of ferroptosis-related markers (Fe, MDA, GSH, and SOD), and improved cognitive performance. In vitro, HT22 neurons exposed to conditioned medium from lipopolysaccharide (LPS)-activated BV2 microglia underwent ferroptotic cell death, which was prevented by ferrostatin-1 but not by apoptosis or autophagy inhibitors. Notably, pharmacological inhibition of the enzymatic activity of class IIa HDACs with TMP269 failed to attenuate ferroptosis, whereas HDAC7 knockdown suppressed P-NF-κB activation, restored MFN2 expression, corrected ACSL4/GPX4 abnormalities, and suppressed ferroptosis, further supporting a deacetylase-independent role of HDAC7. Furthermore, treatment with MASM7, an MFN2 activator, alleviated ferroptosis in vitro without affecting HDAC7 expression or NF-κB phosphorylation. In vivo, MASM7 administration also improved cognitive function and mitigated ferroptosis-related changes after surgery. Taken together, these findings demonstrate that HDAC7 promotes neuronal ferroptosis through the NF-κB-MFN2-ACSL4 pathway, thereby contributing to the development of PND. - Source: PubMed
Publication date: 2026/04/08
Guo JunzuoChi WenyingZhang KaiyunHuang YaruZhang BowenGuo XinleiMeng Fanjun - Histone deacetylase HDAC7 is required for early B cell development and governs the acquisition of B cell progenitors gene identity. Its role in mature B cell biology and associated malignancies is unknown. Here, by using a conditional mouse model for specific deletion in activated B cells, we demonstrate that HDAC7 is essential for the formation of germinal centers (GC). HDAC7 deficiency results in the generation of aberrant GCB cells, diminished class switch recombination (CSR) and plasma cell (PC) formation. We demonstrate that low expression of HDAC7 in diffuse large B cell lymphoma (DLBCL) tumors is associated with poor prognosis of the patients. Importantly, expression of HDAC7 in DLBCL cell lines reduces the proliferative capacity, as well as DLBCL tumorigenicity in vivo. In summary, our data revealed first, the important function of HDAC7 in the establishment of the GC, and second, the potential contribution of HDAC7 deregulation in DLBCL. - Source: PubMed
Meler AinaraGusi-Vives Marde Barrios OriolAzagra AlbaCollazo OlgaMelchor JavierDel Monte-Monge AlbertoGyőrffy BalázsVerdu-Bou MiriamNavarro José-TomásMartín-Subero José IgnacioRoué GaëlRamiro Almudena RRoa SergioParra Maribel - Adenosine-to-Inosine (A-to-I) modification is one of the most common transfer RNA (tRNA) modifications in humans. However, the role of A-to-I tRNA modification in colorectal cancer (CRC) remains poorly understood. - Source: PubMed
Publication date: 2026/03/17
Cheng Cillian HJi FenfenShen JianmingJiao YingChen DanyuYang HuanYe LiufangTao RuizhiWei QinyaoKang WeiYu JunWong Chi Chun