SIRT7 antibody
- Known as:
- SIRT7 (anti-)
- Catalog number:
- orb100696
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SIRT7 antibody
Related genes to: SIRT7 antibody
- Gene:
- SIRT7 NIH gene
- Name:
- sirtuin 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2014-11-19
Related products to: SIRT7 antibody
Related articles to: SIRT7 antibody
- Colorectal cancer (CRC) is a prevalent malignancy with a complex genetic basis. Recent genome-wide association studies (GWAS) have identified a susceptibility locus at 3p21.31, however, the functional SNP(s) underlying the association between the 3p21.31 region and CRC remain to be elucidated. In this study, we identified rs2101247 as the potential functional SNP and further demonstrated that rs2101247 is significantly associated with the expression of the nearby long non-coding RNA (lncRNA) RP11-708J19.2 (ENSG00000271161.1). Functional experiments showed that RP11-708J19.2 is upregulated in CRC tumor tissues, and its knockdown reduces cell viability while promoting apoptosis in SW1116 and HCT116 cell lines. Mechanistically, RP11-708J19.2 interacts directly with the deacetylase SIRT7, modulating histone H3K18 acetylation (H3K18ac). Specifically, RP11-708J19.2 knockdown leads to a significant upregulation of H3K18ac levels, implicating a SIRT7-mediated epigenetic pathway in CRC progression. Our findings elucidate a novel functional SNP-lncRNA axis that contributes to CRC pathogenesis, providing potential biomarkers for early detection and therapeutic targets for intervention. - Source: PubMed
Publication date: 2026/07/23
Ma JialiTian XianglongQiu YiwenZhao ChenWang JinghuiJia Rongrong - Sirtuins (SIRT1-SIRT7) are nicotinamide adenine dinucleotide (NAD) dependent deacylases that serves as metabolic sensors, coupling cellular energy status to chromatin structure, mitochondrial function, and stress responses. Dysregulated SIRT activity has been extensively studied in aging, metabolic syndrome, cardiovascular disease, neurodegeneration, cancer, and immune disorders. However, robust human evidence and SIRT-targeted therapies are lacking. Transgenic mouse models serve as key platforms to study gene function and guide therapeutic development. This review synthesizes evidence from transgenic mouse models regarding the core cellular processes governed by SIRTs: metabolism, genome integrity, stress resistance, immunity, and autophagy, and illustrates their operation across different organ systems. By comparing global, tissue-specific, and inducible knockout (KO) and overexpression (OE) models of cardiovascular, respiratory, digestive, nervous, endocrine, urogenital, musculoskeletal, malignant, and immune diseases, we identified central regulatory SIRTs (SIRT1, SIRT3, and SIRT6), context-dependent modifiers (SIRT2, SIRT4, SIRT5, and SIRT7), and their organ- and cell type-specific functions. We also summarize representative small-molecule SIRT activators, inhibitors, and degraders, covering both clinical and preclinical studies, and highlight where contradictions and knowledge gaps remain. Together, these analyses help clarify which aspects of SIRT modulation are most promising and under what isoform, tissue, and disease contexts they should be pursued for the development of SIRT‑targeted therapies in human disease. - Source: PubMed
Publication date: 2026/07/22
Wang Jia-YiJiang Feng-LiZhang Fang-YuanHuang Dong-HuiLi Xiao-YingGao SongYou HuaWu Qi-JunChen Huan-HuanGong Ting-Ting - Protein succinylation, an emerging post-translational modification (PTM), assumes a crucial role in the initiation and advancement of inflammatory diseases. Ferroptosis, propelled by lethal lipid peroxidation, is intricately associated with the pathogenesis of inflammation. Targeting ferroptosis has recently emerged as a promising therapeutic approach for acute lung injury (ALI). Nevertheless, the crosstalk between protein succinylation and ferroptosis in the regulation of ALI remains ambiguous. FOXO4, a key regulator of oxidative stress responses, is dynamically regulated by various PTMs. We identify SIRT7 as the desuccinylase essential for FOXO4 activation and nuclear localization. Mechanistically, SIRT7 desuccinylates FOXO4 at lysine 139 (K139), thereby inhibiting MDM2-mediated K48-linked polyubiquitination, which stabilizes FOXO4 and maintains FOXO4 nuclear retention. This consequently upregulates glutathione peroxidase 4 (GPX4) and suppresses lipopolysaccharide (LPS)-induced ferroptosis in alveolar epithelial cells (AECs). In vivo experiments demonstrated that SIRT7-knockout (SIRT7-KO) exacerbates LPS-induced ALI. Furthermore, the delivery of a FOXO4-K139R (mimicking desuccinylation) via adeno-associated virus 6 (AAV6) significantly alleviated pulmonary ferroptosis and histopathological damage in SIRT7-KO mice. Notably, pharmacological activation of SIRT7 with trilobatin (TLB) significantly attenuates ALI in LPS-challenged mice, establishing a potential therapeutic pathway for this pathology. Collectively, these findings delineate a previously unrecognized mechanism through which SIRT7 governs the nuclear retention and activation of FOXO4 via desuccinylation, establishing the SIRT7-FOXO4 axis as a potential therapeutic target and theoretical basis for ALI intervention. - Source: PubMed
Publication date: 2026/07/18
Shen KaikaiWei YuqingXu HaoKe ZhangminZhang HeZhou XinyuChen PeilinZhan PingZhang FangZhu SuhuaJin JiajiaLv TangfengSong Yong - Breast cancer (BRCA) is a major health threat to women and often carries a poor prognosis. Succinylation is closely associated with cancer metabolism; however, research on succinylation-related genes (SRGs) in BRCA remains relatively limited. This study first identified differentially expressed genes between normal and BRCA groups in the TCGA cohort and intersected them with known SRGs to obtain differentially expressed SRGs (DE-SRGs). Univariate Cox and LASSO Cox regression analyses were used to screen the DE-SRGs, followed by multivariate Cox regression to develop a succinylation-related prognostic model. Subsequently, patients were categorized into high and low succinylation-related risk score (SRS) groups according to the median score. Two groups were then compared for differences in immune microenvironment characteristics, somatic mutation burden, and drug sensitivity. Additionally, the expression levels of the signature genes were validated via qRT-PCR. This study developed a prognostic risk model for BRCA patients based on 13 SRGs (ACOT4, ALDH3A1, B3GALT1, IFNG, MMP1, NFKB2, PCSK6, PTK2, SERPINA1, SHMT2, SIRT7, ST3GAL1, and SUCLA2). A markedly elevated infiltration of immune cells was observed in the low-SRS group, including B cells, Mast cells, and Macrophages. The tumor mutational burden was notably lower in the low-SRS group. Drug sensitivity analysis suggested that the high-SRS BRCA patients might be more susceptible to FTI-277 and GNF-2. qRT‑PCR results showed that ACOT4, IFNG, MMP1, NFKB2, PCSK6, PTK2, SHMT2, SIRT7, and ST3GAL1 were significantly upregulated in human BRCA cell lines, while ALDH3A1, B3GALT1, and SUCLA2 were significantly downregulated. Our findings highlight the prognostic value of SRGs in BRCA, laying the groundwork for its potential use in guiding personalized treatment. - Source: PubMed
Publication date: 2026/07/17
Chen ZhifengHu Mi - Neurodegenerative diseases are characterized by progressive neuronal loss driven by protein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Among these, Parkinson's disease (PD) is a prevalent disorder marked by degeneration of dopaminergic neurons in the substantia nigra and the accumulation of α-synuclein aggregates. Emerging evidence indicates that mitochondrial dysfunction and metabolic dysregulation are central contributors to PD pathogenesis. Sirtuins (SIRT1-SIRT7), a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, have emerged as key regulators of neuronal survival and metabolic homeostasis. Mechanistically, SIRT1 regulates α-synuclein aggregation, autophagy, and neuroinflammatory signaling, while SIRT3 preserves mitochondrial integrity and reduces oxidative stress. In contrast, SIRT2 has been implicated in microtubule destabilization and neurotoxicity, and its inhibition has demonstrated neuroprotective effects in experimental models. This review provides a comprehensive, up-to-date synthesis of the molecular mechanisms underlying sirtuin-mediated neuroprotection in PD and related neurodegenerative disorders. We further discuss the translational potential of targeting sirtuin pathways, including pharmacological modulators and NAD+-boosting strategies, while addressing current limitations and future directions for clinical translation. - Source: PubMed
Publication date: 2026/07/17
Kumari ShobhaSingh HemrajVaidya ShravaniTaliyan Rajeev