SIRT2
- Known as:
- SIRT2
- Catalog number:
- 000468A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SIRT2
Ask about this productRelated genes to: SIRT2
- 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
Related articles to: SIRT2
- Accumulating evidence indicates that reversible acetylation modifications are critically involved in the regulation of gene expression, metabolic pathways, and the tachyzoite transformation in Toxoplasma gondii. Silent information regulator 2 (SIR2), an NAD-dependent lysine deacetylase, contributes to the maintenance of specific silent chromatin domains in mammals. However, its exact functions in T. gondii are unclear. In this study, we systematically analyzed two SIR2 homologs, TgSIR2A, and TgSIR2B, in T. gondii. Our findings demonstrate that TgSIR2A exerts a more pronounced effect on tachyzoite growth compared to TgSIR2B. TgSIR2A is predominantly localized in the cytoplasm of tachyzoites and exhibits cell cycle-dependent expression. Conditional depletion of TgSIR2A significantly impairs tachyzoite invasion. Using gain- and loss-of-function approaches, we confirmed that the histidine at position 228 is essential for TgSIR2A's catalytic activity. Mutation of this residue elevates global acetylation levels and compromises tachyzoite invasion capacity. Furthermore, acetylated proteomics and interaction analyses suggest that TgSIR2A may regulate gene expression, protein translation, and maturation processes in tachyzoites. Notably, TgBip, an ER-associated chaperone, may be a substrate of TgSIR2A. Collectively, our results indicate that TgSIR2A plays an important role in tachyzoite invasion via its lysine deacetylase activity, making it a potential target for treating T. gondii infections. - Source: PubMed
Wu YantaoLiu XiaonaTian XinXie YangyangWu YunjiaZheng XiaoziHu XinHua QianqianZhao WeiMou YaniTan Feng - Chronic liver injury progressively induces fibrotic remodeling through persistent inflammatory activity and aberrant extracellular matrix accumulation. Growing evidence indicates that this process involves not only intrahepatic signaling but also gut-liver crosstalk and sirtuin-regulated inflammatory pathways. Hesperetin, a citrus-derived flavanone with reported antioxidant and anti-inflammatory properties, has not been adequately evaluated with respect to microbiota-associated changes and SIRT2-associated signaling during fibrotic liver injury. - Source: PubMed
Publication date: 2026/06/17
Wu AnzhaoXin LingjieLiang YujiSun LuyanLiu QianWang BinLi YaPingCui YuehongSaeed UmarYang BoZahid Piracha Zahra - White spot syndrome virus (WSSV) is a major pathogen in shrimp aquaculture, yet how virus-induced metabolic rewiring alters immune effector function remains poorly understood. Here, we show that WSSV infection in Litopenaeus vannamei induces a Warburg-like metabolic shift characterized by increased glucose uptake, transcriptional activation of glycolytic genes, lactate accumulation, and reduced acetyl-CoA levels. This metabolic state is accompanied by enhanced lactylation and reduced acetylation of hemocyanin, a major respiratory and immune protein in shrimp. Through transcriptome-guided candidate screening and in vivo RNA interference, we identify Tip60 as a positive regulator of hemocyanin lactylation, whereas HDAC3 and SIRT2 act as negative regulators. Functional assays further demonstrate that hemocyanin samples isolated from sodium L-lactate-injected shrimp exhibit enhanced capacities to increase cell-associated WSSV on hemocytes and promote viral proliferation. Together, these findings support a model in which WSSV hijacks host glycolytic reprogramming to reshape the post-translational modification landscape and convert hemocyanin into a proviral factor. This study establishes a non-histone lactylation mechanism in crustacean antiviral biology and identifies the Tip60/HDAC3/SIRT2 axis as a potential target for host-directed control of WSSV infection. - Source: PubMed
Publication date: 2026/09/10
Ren XinyueChen BaiqiaoLuo KaiZhou YayanWu YuxiJiang MingmingZhang ZiyiZhang YinghaoLv YuqingZhang YuelingZheng Zhihong - Cellular pathways for experimental discovery provide a comprehensive overview of sirtuin biology and its critical involvement in HIV-associated neurocognitive disorders (HAND) and related neurodegenerative diseases, highlighting the translational potential of sirtuin-targeted therapeutic strategies. As NAD-dependent deacetylases and ADP-ribosyl transferases, sirtuins regulate diverse cellular processes, including stem cell maintenance, cellular proliferation, metabolic homeostasis, apoptosis, autophagy, oxidative stress responses, and genomic stability, all of which contribute to neuronal dysfunction and disease progression. This chapter focuses on key mammalian sirtuins, including SIRT1 and SIRT2, which are primarily localized within the nucleus and cytosol; mitochondrial sirtuins SIRT3, SIRT4, and SIRT5; and nuclear/nucleolar sirtuins SIRT6 and SIRT7. Here, a method with a detailed protocol to isolate compartment-specific sirtuin expression and activity was used: subcellular fractionation was performed using a subcellular fractionation kit to obtain cytosolic and nuclear fractions, while mitochondrial isolation was carried out using Tom20 antibody-conjugated magnetic microbeads. These approaches were applied to brain tissues from HIV-positive individuals, as well as to HIV-Tat-treated human microglial (HMC3) cells and astrocytes. This experimental framework enables accurate assessment of compartment-resolved sirtuin regulation in disease-relevant models. Collectively, the chapter highlights the protective roles of sirtuins in mitigating key pathogenic mechanisms underlying HAND and related neurodegenerative diseases. These findings support the emerging concept that sirtuins represent promising pharmacological targets for the development of novel therapeutic interventions in neurodegeneration and HIV-associated brain disorders. - Source: PubMed
Publication date: 2026/07/13
Chennakesavan KarthickSamikkannu Thangavel - Acute pancreatitis (AP) is a potentially life-threatening inflammatory disorder characterized by trypsin overactivation within acinar cells. While SIRT2 is linked to inflammation, its precise role in AP remains poorly understood. - Source: PubMed
Publication date: 2026/08/31
Ma Shi-YaShen Zhao-JianZhu Chong-ZhiShen CuiLu Zhong-HuaSun YunYu Wei-Li