SIRT6 antibody - middle region (ARP32408_P050)
- Known as:
- SIRT6 (anti-) - middle region (ARP32408_P050)
- Catalog number:
- arp32408_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SIRT6 antibody - middle region (ARP32408_P050)
Related genes to: SIRT6 antibody - middle region (ARP32408_P050)
- Gene:
- SIRT6 NIH gene
- Name:
- sirtuin 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2015-09-02
Related products to: SIRT6 antibody - middle region (ARP32408_P050)
Related articles to: SIRT6 antibody - middle region (ARP32408_P050)
- - Source: PubMed
Publication date: 2026/04/18
Leng ShuaiLiu WenyanHan YuDang ZhiqiaoZhang FengquanYu Wenqian - Cellular senescence, frequently driven by excess reactive oxygen species (ROS), is a major contributor to organismal aging. Anti-aging strategies that reduce ROS often show limited efficacy due to poor bioavailability of therapeutics, and the development of more effective anti-senescent agents remains an important research objective. In this study, we sought to integrate the activity of resveratrol (RSV), a polyphenolic antioxidant with documented anti-senescence properties, with the (2,2,6,6-tetramethylpiperidin-1-yl)oxyl radical (TEMPO), a superoxide dismutase mimetic. While RSV and TEMPO display synergistic radical-scavenging activity in chemical model systems, this effect is not reproduced in cellular environments, likely due to their divergent subcellular localization. To overcome this limitation, a hybrid molecule, termed H3, was synthesized by covalently linking RSV with TEMPO to integrate the properties of both components within a single molecular framework. H3 exhibited potent radical-trapping antioxidant activity in all chemical assays employed. In human dermal fibroblasts, H3 was non-cytotoxic and significantly attenuated multiple hallmarks of senescence, maintaining DNA replication competence and reducing the proportion of senescent cells. H3 surpassed the efficacy of RSV, TEMPO, and their equimolar mixture in preserving cellular proliferation. Under oxidative stress, H3 maintained the expression of central antioxidant enzymes, including SOD1, CAT, and HO-1. In fibroblasts induced to senescence, H3 upregulated lamin B1, PARP, SirT1, and SirT6-proteins essential for chromatin organization, genome stability, and DNA repair. As a result, H3 is an anti-senescent agent, combining direct radical-trapping activity with the ability to influence the expression of antioxidant defense and DNA repair proteins. - Source: PubMed
Publication date: 2026/04/14
Konopko AdrianSęktas KatarzynaTargońska AlicjaAmorati RiccardoBielak-Zmijewska AnnaLitwinienko Grzegorz - Consumption of var. has antioxidant and hypoglycemic effects. Regarding the former, certain signaling pathways that influence these effects have already been proposed; however, the underlying molecular mechanisms of the hypoglycemic effects remain unknown. It has been recognized that the sirtuin-mediated signaling cascade responds to various stressors, such as oxidative stress, and regulates glucose metabolism. Therefore, it would be of great interest to determine whether there is a link between these two properties and whether it is mediated by sirtuins. Hence, the present study aimed to evaluate the effect of on the gene expression of the sirtuin family (SIRT1-SIRT6) in individuals with type 2 diabetes mellitus (T2DM). A quasi-experimental study was conducted with a convenience sample of 26 older adults diagnosed with T2DM, divided into a (i) placebo group (PG; = 14) and (ii) experimental group (EG; = 12). Clinical, biochemical, and anthropometric measurements were performed, and total oxidant/antioxidant capacity (TOS/TAS) and mRNA expression of genes encoding sirtuins were determined. All parameters were measured at baseline, three months, and six months after the intervention. In the EG, the expression levels of SIRT1, SIRT3, SIRT5, and SIRT6 increased by 52%, 69%, 62%, and 69%, respectively, six months after treatment. A 50% decrease in TOS and a 44% increase in TAS were also observed. Our findings suggest that the bioactive components of enhance sirtuin expression and exhibit antioxidant effects in older adults with T2DM. - Source: PubMed
Publication date: 2026/04/02
Gavia-García GracielaHernández-Álvarez DavidArista-Ugalde Taide LauritaAguiñiga-Sánchez ItzenSantiago-Osorio EdelmiroCadena-Iñiguez JorgeRosado-Pérez JuanaMendoza-Núñez Víctor Manuel - Sirtuin 6 (SIRT6), belong to the NAD-dependent class III protein deacetylase family, is implicated in cancer development through a multifaceted role. While it has been identified with both tumor-suppressive and tumor-promoting roles in Hepatocellular carcinoma (HCC), there remains considerable debate regarding its exact function. The specific molecular mechanisms driving its tumor-suppressive effects in HCC remains poorly understood. In this study, we mechanistically identified a novel pathway involving AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and transcription factor EB (TFEB): upregulation of SIRT6 enhances AMPK activity and suppresses mTOR activation, leading to TFEB nuclear translocation and the subsequent induction of autophagy. Importantly, our study provides the first evidence that SIRT6 induces the translocation of TFEB into the nucleus, facilitating autophagy. Intriguingly, SIRT6 silencing counteracted the effects of mTOR inhibitors on TFEB and autophagy, suggesting that SIRT6 probably activates lysosome function via an AMPK-mTOR-TFEB axis in HCC. Our in vivo experiments bolster our findings, demonstrating that SIRT6 effectively suppressed HCC tumor growth and metastasis. Overall, our research provides compelling evidence that SIRT6 functions as a tumor suppressor in HCC, offering a valuable therapeutic mechanism for treating HCC and paving the way for a promising avenue in future HCC treatment. Schematic illustration of SIRT6's role in hepatocellular carcinoma. Proposing a model to elucidate the regulatory mechanism of SIRT6-AMPK-mTOR-TFEB signaling axis in orchestrating autophagy activation within hepatocellular carcinoma. Phosphorylation of AMPK by SIRT6 leads to the inhibition of mTOR and its downstream targets. This modulation influences TFEB, promoting its translocation into the nucleus and triggering autophagy activation. This intricate cascade is marked by a significant increase in substrate degradation and the formation of autophagic bilayers, ultimately culminating in the suppression of cell proliferation and the augmentation of cell death. - Source: PubMed
Publication date: 2026/04/09
Li Cong ShanJin HuaMeng RuoyuBaek Seung-WooKim Seong-HunChai Ok HeePark Byung HyunLee Ju-SeogLee Na RiKim Soo Mi - Protein acetylation is increasingly recognized as a key regulator of tumor progression, yet natural compounds capable of modulating this modification remain poorly defined. Apigenin, a dietary flavonoid suppresses bladder cancer progression based on functional assays and dynamic xenograft models. Mechanistically, we applied an integrated multi-omics approach to unravel that apigenin enhances SIRT6-mediated deacetylation of Nuclear Receptor Coactivator 2 (NCOA2), leading to site-specific deacetylation of NCOA2 at lysine 780 and 785. This modification potentiates PPARα transcriptional activity, reprograms cellular energy metabolism, and disrupts mitochondrial membrane potential. Clinically, reduced SIRT6 expression coupled with elevated NCOA2 and mitochondrial/β-oxidation markers correlates with metastatic progression in bladder cancer. Together, these findings identify a previously unrecognized SIRT6-NCOA2-PPARα signaling axis as a metabolic vulnerability in bladder cancer. - Source: PubMed
Publication date: 2026/02/26
Liu YingShi Zhen-DuoWei Yun-FeiJiang Si-YuanPatel HarshLiu Qian-ZiDong YangLiu Yi-FangHao LinGao ShanYang Dong-HuaLi QiangHan Cong-Hui