Ask about this productRelated genes to: SIRT1 antibody
- Gene:
- SIRT1 NIH gene
- Name:
- sirtuin 1
- Previous symbol:
- -
- Synonyms:
- SIR2L1
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2016-10-05
Related products to: SIRT1 antibody
Related articles to: SIRT1 antibody
- Vision-threatening ocular diseases are impacted by aging-associated molecular changes, including mitochondrial dysfunction, cellular senescence, and chronic inflammation. Anti-VEGF therapies targeting VEGF-A/VEGFR2 signaling remain the frontline standard of care, but many patients exhibit suboptimal or nondurable responses, often due to compensatory and/or compromised antiangiogenic and anti-inflammatory pathways. We aimed to elucidate shared mechanisms underlying treatment failure and disease progression. - Source: PubMed
Piroozmand SomayehLatifi-Navid HamidSoheili Zahra-SoheilaHosseinkhani SamanSamiei ShahramBarzegar Behrooz AmirAhmadieh HamidLeonardi AndreaGhavami SaeidSheibani Nader - Nearly thirty years ago, T-lymphokine-activated killer (T-LAK) cell-originated protein kinase (TOPK), also known as PDZ-binding kinase, was first identified as a serine/threonine kinase with limited known functions. Over time, this molecule has gradually revealed a far more striking role in cancer biology. Initially detected mainly in proliferative tissues such as testes and activated lymphocytes, TOPK is now recognized as a protein that becomes aberrantly overexpressed in many human cancers, where it is consistently linked to aggressive tumor behavior and poor clinical outcomes. Research accumulated over the past three decades shows that TOPK governs a wide range of oncogenic processes, including proliferation, metastasis, cell cycle progression, DNA damage repair, resistance to apoptosis, autophagy regulation, inflammatory signaling, and immune modulation. Mechanistic studies reveal that TOPK communicates extensively with major signaling molecules such as extracellular signal-regulated kinase (ERK), β-catenin, the tyrosine-protein kinase Src/glycogen synthase kinase 3 beta/signal transducer and activator of transcription 3 (Src/GSK3β/STAT3), phosphoinositide 3-kinase/phosphatase and tensin homolog/protein kinase B (PI3K/PTEN/AKT), TGF-β/small mother against decapentaplegic (SMAD), NF-κB/Snail, and HIF-1α. Positive feedback interactions with ERK2, Src and other oncogenic regulators further intensify its tumor-promoting activity. TOPK also contributes to resistance to anti-cancer agents such as doxorubicin, gefitinib, oxaliplatin, and sorafenib through its influence on activator protein-1, phosphatase and tensin homolog, sirtuin 1 (SIRT1), p53, and additional downstream effectors. In the tumor immune microenvironment, TOPK enhances programmed cell death ligand 1 (PD-L1) expression and reduces CD8 T-cell infiltration, promoting immune evasion. Although numerous natural and synthetic inhibitors of TOPK have been identified, their clinical application remains at an early stage. Overall, current evidence presents TOPK as a promising biomarker and therapeutic target with broad relevance across diverse cancer types. - Source: PubMed
Publication date: 2026/03/31
Zhao MengyuZhao RanDong ZigangLee Mee-Hyun - Type 2 asthma is characterized by airway inflammation, mucus hypersecretion, and remodeling, and circadian rhythm dysregulation is implicated in its pathogenesis. Melatonin, a key circadian hormone, modulates inflammatory signaling, but its role in type 2 airway inflammation remains unclear. This study investigated whether melatonin alleviates airway inflammation and epithelial-mesenchymal transition (EMT) through the melatonin receptor 1 (MT1)-Sirtuin 1 (Sirt1) signaling pathway and circadian clock regulation. - Source: PubMed
Publication date: 2026/04/17
Zhang ZheJiang JieChen GuilianZhang XiuqinWang JipengWang Baolan - Steroid-induced osteonecrosis of the femoral head (SONFH) is a terrible side effect of glucocorticoid therapy that causes problems with microvascular integrity, lipid metabolism, and a range of programmed cell death pathways. Recent studies have shown that autophagy can have different effects on osteoblasts and endothelial cells depending on the situation. These effects are mediated by the AMPK/mTOR, PINK1/Parkin, SIRT1/FoxO1, and PI3K/Akt/mTOR pathways. At the same time, apoptosis is caused by lowering Wnt/β-catenin, raising STAT1/caspase-3, and throwing off the balance of the OPG/RANKL/RANK axis. This makes it harder for bones to develop and makes osteoclasts work too hard. The growing contributions of ferroptosis (SLC7A11/GPX4 axis), necroptosis (RIPK1/RIPK3/MLKL), oxidative stress (NOX-JNK-c-Jun and Keap1-Nrf2), and pyroptosis (NLRP3/Caspase-1 and Caspase-4/5/11 inflammasomes) show that there is a complex network of cell death that makes SONFH worse. Preclinical treatments such as rapamycin, puerarin, lithium, NAC, necrostatin-1, luteolin, MCC950, antler peptides, and FGF23 inhibitors show promise in working together to change these pathways. A better knowledge of pathway crosstalk and dosage-dependent effects is the first step toward tailored, multi-modal therapeutics that can stop and treat SONFH. This review article looks at the signalling pathways that are currently thought to be involved in the pathogenesis of SONFH. Its goal is to help people better understand the disease and how to avoid and treat it more effectively. - Source: PubMed
Publication date: 2026/04/30
Niu XiaojuanLi JunYan ZhongshengChen TiantianYan XiangyongWang JianChen Guangyan - Ultraviolet A (UVA) radiation induces oxidative stress and mitochondrial dysfunction in dermal fibroblasts, contributing to photodamage and skin aging. This study investigated the protective effects of Yeast/rice fermentation filtrate (RFF) and sialic acid (SA), both individually and in combination, against UVA-induced damage in human dermal fibroblasts. Cell viability, reactive oxygen species (ROS) levels, intracellular ATP and NAD contents, and mitochondrial membrane potential (ΔΨm) were evaluated following treatment. RFF, SA, and their combination significantly improved cell viability in UVA-damaged fibroblasts and reduced ROS generation. Notably, the combined treatment increased intracellular ATP levels by 201.2% ( < 0.05), with enhancements of 62.3% and 285.4% compared to RFF and SA alone, respectively. Additionally, the combined treatment significantly restored NAD levels and effectively preserved mitochondrial membrane potential. Transcriptomic analysis revealed modulation of pathways related to cellular energy metabolism, particularly AMPK, and upregulation of SIRT1, SIRT3, and SIRT5 expression. The RFF-SA combination confers robust UVA photoprotection by enhancing mitochondrial resilience, providing a foundation for the development of protective cosmetic formulations. - Source: PubMed
Publication date: 2026/04/11
Yang FanLi MingxuanZuo YaoGuo MiaoLiu ZhiWang Hua