SIRT2 antibody - N-terminal region (ARP32384_T100)
- Known as:
- SIRT2 (anti-) - N-terminal region (ARP32384_T100)
- Catalog number:
- arp32384_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SIRT2 antibody - N-terminal region (ARP32384_T100)
Related genes to: SIRT2 antibody - N-terminal region (ARP32384_T100)
- 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 - N-terminal region (ARP32384_T100)
Related articles to: SIRT2 antibody - N-terminal region (ARP32384_T100)
- To identify candidate biomarkers of blood stasis syndrome (BSS) associated with coronary artery disease (CAD) and explore the underlying inflammatory mechanisms. - Source: PubMed
Hongzheng L IGuosheng LinYuxuan PengAlexey Viktorovich ChurovWenwen YangJie WangJieming L UFeifei LiaoRuotong Y UYue WeiZhiru ZhaoAimei L UPeng L IAling ShenLinzi LongHua Q UChanggeng F U - Increased silent information regulator protein 2 (SirT2) expression in the prefrontal cortex (PFC) has been reported to be associated with the development of depression; however, its functional contribution to depression-like behavior and memory impairment remains incompletely understood. In this study, we examined alterations in SirT2 expression in the PFC of olfactory bulbectomized (OBX) mice, a well-established model of depression, and evaluated the effects of AK-7, a selective SirT2 inhibitor, on OBX-induced depression-like behavior and memory impairment. On day 21 after surgery, OBX mice exhibited depression-like behaviors and memory impairment, as evidenced by prolonged immobility, reduced sucrose preference and spontaneous alternation, and shortened passive avoidance latency. Expression of SirT2 and pro-inflammatory microglial markers increased significantly, while those of Ac-FoxO1, PPARγ, arginase-1, MBP, MAG, CNPase, and Caspr were decreased, in the PFC of OBX mice. AK-7 administration attenuated these behavioral and molecular alterations. SirT2, Ac-FoxO1, and PPARγ showed spatial overlap with the microglial marker Iba1. AK-7 reduced microglial activation-associated morphological changes and attenuated OBX-induced disruption of node of Ranvier formation. These results suggest that AK-7 administration attenuates depression-like behavior and memory impairment, with concurrent improvements in node of Ranvier organization and modulation of microglial polarization in the PFC. Furthermore, our findings suggest that dysregulated SirT2 signaling may be involved, at least in part, in the development of depression-like behavior and comorbid memory impairment, and represents a potential avenue for further investigation. - Source: PubMed
Publication date: 2026/04/21
Takahashi KoheiKurokawa KazuhiroHiraga DaikiTakeda HiroshiTsuji Minoru - The human NAD (+)-dependent deacetylase silent information regulator isoform 2 (SIRT2) is the cytoplasm-localized member of the sirtuin family, which has received increasing attention for its potential roles in cancer diagnosis and therapy. However, its role is still under debate, and its molecular mechanism remains unclarified. In this study, we thoroughly investigated the function and regulatory mechanism of SIRT2 in the tumorigenesis of liver cancer and found that SIRT2 is highly expressed in liver cancer tissues and is distributed mainly in the cytoplasm of liver cancer cells. The SIRT2 expression level is positively related to cell proliferation in vitro and tumour growth in vivo. We found that SIRT2 can upregulate IGFBP1 expression and subsequently activate the PI3K/AKT/mTOR signalling pathway and that IGFBP1 is essential for the tumour-promoting function of SIRT2 in liver cancer. Moreover, we characterized that dihydroartemisinin, one of the main active metabolites of artemisinin derivatives can inhibit liver cancer cell proliferation and liver tumour growth by promoting ubiquitin-dependent SIRT2 degradation and subsequently blocking SIRT2-IGFBP1-induced PI3K/AKT/mTOR signal pathway. - Source: PubMed
Publication date: 2026/04/20
Chai ZhengbinLiu JingwenLiu JingNiu LinfeiWang XiaoqingLiu ChunyanHan Fabin - Selective inhibitors of the nicotinamide adenine dinucleotide (NAD⁺)-dependent lysine deacylase sirtuin 2 (SIRT2) have emerged as promising therapeutics, as SIRT2 is increasingly recognized as a critical regulator in the pathogenesis of cancer and neurodegenerative diseases. Moreover, the development of selective SIRT2 inhibitors provides valuable insights into the physiological and pathophysiological roles of this enzyme, thereby contributing to both mechanistic understanding and therapeutic strategies for these disorders. Accordingly, our sustained efforts to identify selective SIRT2 inhibitors have resulted in a structurally diverse in-house library of small-molecule compounds. In this study, the inhibitory activities of 69 in-house compounds were evaluated as percentage inhibition at a fixed concentration of 100 µM and converted to a logarithmic scale to serve as a screening metric for a three-dimensional quantitative structure-activity relationship (3D-QSAR) modeling. The generated 3D-QSAR model, based on molecular field analysis, yielded statistically significant results (R=0.8251, Q=0.7888, and Pearson-r = 0.8917) and enabled the identification of key structural features responsible for inhibitory activity. Our findings highlight the significance of steric and hydrophobic features in SIRT2 inhibition. Furthermore, the generated contour maps indicated favorable and unfavorable regions for incorporating electrostatic, hydrogen bond acceptor (HBA), hydrogen bond donor (HBD) groups, and aromatic rings to improve the targeted activity. - Source: PubMed
Publication date: 2026/04/09
Ozgencil FikriyeEren Gokcen - : Sirtuin-2 (SIRT2) is a longevity-related protein implicated in apoptosis, metabolic regulation and oxidative stress; however, its role in ageing pancreas remains unclear. : This study investigated the effects of the selective SIRT2 inhibitor, Arabidopsis guanylate kinases-2 (AGK-2) on oxidative stress and apoptosis in aged rat pancreatic tissue. : Young (3-month) and aged (22-month) rats were divided into control and AGK-2-treated groups (10 μM, 30 days). Total oxidant status (TOS) and total antioxidant status (TAS) used commercial kits, then calculated Oxidative stress index (OSI). For detecting nitrosative stress, we determined nitrite-nitrate levels using the Griess test. SIRT2 and caspase-3 were evaluated by ELISA and Western blot. : Our findings showed that ageing increased SIRT2 expression, oxidative stress and caspase-3 protein compared to young rats. AGK-2 treatment reduced SIRT2, TOS, OSI and caspase-3, and increased TAS particularly in aged rats. AGK-2 reverses ageing-associated changes in pancreatic oxidative stress and apoptosis. SIRT2 modulation may represent a potential therapeutic target against age-related pancreatic degeneration. - Source: PubMed
Publication date: 2026/04/17
Bakal Muratoğlu SaideKeskin Aktan ArzuBabahan CansuAkbulut K Gonca