SIRT2 Antibody
- Known as:
- SIRT2 Antibody
- Catalog number:
- 32057
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- SIRT2 Antibody
Related genes to: SIRT2 Antibody
- Gene:
- SIRT2 NIH gene
- Name:
- sirtuin 2
- Previous symbol:
- SIR2L
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2016-10-05
Related products to: SIRT2 Antibody
Related articles to: SIRT2 Antibody
- Sirtuin-2 (SIRT2) is a cellular deacylase, regulating cell cycle progression and metabolic homeostasis. Recently, SIRT2 has emerged as a target with both anticancer and antiviral potential. However, the role and targetability of SIRT2 in viral-driven cancers remains unexplored. Epstein-Barr virus (EBV) is a ubiquitous herpesvirus with oncogenic potential that establishes latency in B lymphocytes and is typically controlled by a robust T cell immune response. In settings that compromise this response, such as immune suppression following transplant, EBV can cause B cell lymphomas. With broad immunosuppression and varying response rates limiting the effectiveness of existing lymphoma therapeutics, new strategies are necessary. Here, we report that SIRT2-selective compounds block EBV-mediated B cell transformation and EBV or mitogen-driven B cell division in vitro. SIRT2 modulation significantly alters gene expression and metabolism of EBV-infected B cells, reducing mitochondrial respiration, driving mitochondrial swelling, and inducing nutrient stress and autophagy. Treatment with SIRT2 modulators drives hyperacetylation of targets involved in lipid metabolism, central carbon metabolism, and oxidative phosphorylation. EBV-positive and EBV-negative B cell lymphomas rely on glycolysis to avoid cell death after SIRT2 modulation, revealing a metabolic vulnerability that can be harnessed to kill lymphoma cells. Overall, we have identified how SIRT2 could be implicated as a target of therapeutic potential for B cell lymphomas, while also defining fundamental roles for extranuclear lysine acetylation in regulating B cell proliferation and metabolism. - Source: PubMed
Publication date: 2026/08/24
Hill Kaeden KBarry Ashley PReinoso-Vizcaino Nicolas MHaynes Lauren EBonglack Emmanuela NFerreira Davis FMiller Sara EHirschey Matthew DChiang Lillian WRemiszewski StacyLuftig Micah A - Enhancement of the splenic function by preserving its cellular/junctional integrity is an underrated effective strategy in combatting infections. The present work aimed to assess the effect of sirtuin (Sirt) modulation in splenic dysfunction associated with lipopolysaccharide (LPS)-induced endotoxemia in rats. Endotoxemia was induced by a single LPS injection (10 mg/kg; i.p) either solely or preceded by one of 2 Sirt modulators for 3 days; AGK2 (41 mg/kg/d; i.p) or resveratrol (RSV; 40 mg/kg/d; i.p). The results revealed an existing association between AGK2-mediated Sirt-2 inhibition and wingless homolog Wnt5a refining with contemporaneous stimulation of the splenic receptor tyrosine kinase like orphan receptor-2/Frizzled-4/Dishevelled-2 axis. This coincided with enhancement of the planar cell polarity stream (PCP) components, namely, Guanosine-5'-triphosphate-bound Ras homolog family member-A/rho-associated coil-containing protein kinase-1/2, that was in turn linked to augmentation of splenic VE-cadherin content and immunohistochemical expression and instigation of focal adhesion kinase activating phosphorylation. These events were accompanied by enhanced splenic count of differentiated T cells to halt the plasma endotoxin increment with partial suppression of the resultant cytokine storm. The biochemical amendment was further validated by restoration of splenic macro- and microscopic architecture, improved survival and clinical outcomes, and amelioration of end-organ damage markers. Resveratrol failed to achieve such remarkable effects; a conclusion that might be attributed to the hinderance of its anti-inflammatory actions by its Sirt-2 activating capacity, leading to eventual mild endotoxin level decrement in the experimental model. The Sirt2 selective inhibition might be superior in renovating splenic patterning by fine-tuning the Wnt5a/PCP axis and reconstructing junctional scaffolding that functions to expand the blood filtration capacity, besides, immune cells synthesis and migration, presenting a novel approach to conquer the underlying endotoxemia. - Source: PubMed
Publication date: 2026/08/24
Zaky Doaa AAhmed Lamiaa AMohamed Yasmin S - Ferroptosis is a non-apoptotic form of cell death characterized by cellular accumulation of iron-dependent lipid peroxidation. In recent years, a series of studies have proved that ferroptosis participate in the progression of chronic kidney disease (CKD). Notably, cognitive dysfunction is commonly found in CKD patients and it has been recognized as one of CKD pathological features. However, the character of ferroptosis in CKD related cognitive dysfunction remains unclear. This study aims to verify if ferroptosis participates in the CKD related cognitive dysfunction and the underlying mechanism. Then we use Fer-1 and Erastin to explore the effects of ferroptosis on cognition changes in CKD rat. RNA-seq analysis identified ferroptosis related lipid metabolism was significantly changed in CKD rats and the DEGs played an important role in oligodendrocyte differentiation, which were correlated with cognition ability. Fer-1 ameliorated the ultrastructure of hippocampal CA1 region and rescued the myelin sheath injury in CKD rats. Specifically, Fer-1 increased the density of myelinated axons and upregulated the levels of MBP and SOX10 in hippocampus of CKD rats. Notably, Fer-1 decreased the expression of Sirt2 and the AAV-Sirt2 abrogated the beneficial effects of Fer-1 on ferroptosis and myelin sheath in the hippocampus of CKD rats. This study provides a new strategy for improving cognitive dysfunction in CKD. - Source: PubMed
Publication date: 2026/08/15
Yu HuanZhang Chao-YangCai YanLiu YingWu NingWang Wen-JuanCai Guang-YanWang Yuan-Cheng - Age-related metabolic dysregulation, chronic inflammation, and impaired vascularization severely compromise critical-sized bone healing. Building upon G-PLA nanocomposites previously established for bioelectronic encapsulation, we herein investigate their potential as a bio-instructive interface for guided bone regeneration. Fabricated via in situ graphite exfoliation, G-PLA provides enhanced hydrophilicity, mechanical robustness, and bioactivity while preserving excellent 3D-printability. In rat cranial defects, G-PLA significantly accelerated regeneration, as demonstrated by micro-CT, histological, and immunohistochemical analyses. Comparative evaluations in young and aged animals revealed that G-PLA effectively mitigates age-dependent declines in reparative capacity. Proteomic profiling indicated that G-PLA orchestrates a pro-regenerative microenvironment by inducing glycolytic reprogramming to meet the elevated energy demands of regeneration. In aged defects, G-PLA upregulated glycolytic enzymes (e.g., ALDOA and HK2), enhanced angiogenesis (CD31/CD34), and suppressed inflammation- and senescence-associated markers (e.g., P21 and SIRT2). In vitro studies validated that G-PLA augments glycolytic flux in endothelial cells, enhances osteogenic differentiation of mesenchymal stem cells, and promotes macrophage polarization toward an anti-inflammatory M2 phenotype. Therefore, G-PLA nanocomposites transcend passive structural support to act as a bio-instructive interface that revitalizes the aging-associated vascular-bone coupling, offering a versatile framework for next-generation multifunctional implantable hybrid systems. - Source: PubMed
Publication date: 2026/08/13
Wang MengjiaZhang YanghengPan HaiyangXu ShuoyangZou YantingPeng ZhiweiJiang HaichangZhu ZhenYang WenrongLi YanfenSun LitaoHong HuaYan Fuhua - Sirtuins (SIRTs) are NAD-dependent enzymes implicated in cancer and other diseases, but the high conservation of their catalytic sites complicates the development of isoform-selective inhibitors. BZD9L1 is a benzimidazole-based sirtuin inhibitor with previously reported activity against SIRT1 and SIRT2. However, its potential interactions with other human sirtuin isoforms remain incompletely characterized. Here, we applied a comparative structure-based modelling framework integrating homology modelling, molecular docking, and targeted experimental assessment to investigate plausible binding modes of BZD9L1 across human SIRT1-7. Docking predicted that BZD9L1 could occupy the ADP-ribose cofactor-binding region of all seven isoforms, with broadly conserved orientations but differences in the predicted interaction networks. Hydrogen-bonding and π-mediated contacts predominated in the selected SIRT1-3 poses, whereas hydrophobic contacts were more apparent in several selected SIRT4-7 poses. The modest differences in docking scores were interpreted qualitatively and do not establish differential binding affinities or isoform selectivity. In colorectal cancer cells, BZD9L1 treatment altered acetyl-SOD2 levels, consistent with altered SIRT3-associated deacetylation in a cellular context. In a separate cell-free enzymatic assay, no measurable SIRT5 inhibition was detected under the conditions tested. These complementary assays provided distinct, independently interpreted readouts of SIRT3-associated cellular activity and SIRT5 enzymatic activity. Collectively, this study provides testable structural hypotheses regarding BZD9L1 recognition by human sirtuins and identifies interaction features that may guide subsequent biochemical and structure-based investigations. - Source: PubMed
Publication date: 2026/07/30
Tan Yi JerLee Yeuan TingOon Chern EinMancera Ricardo L