Human Polyclonal SIRT1 Ab
- Known as:
- Human Polyclonal SIRT1 Antibody
- Catalog number:
- a0230
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal SIRT1
Related genes to: Human Polyclonal SIRT1 Ab
- 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: Human Polyclonal SIRT1 Ab
Related articles to: Human Polyclonal SIRT1 Ab
- The protein histone deacetylase silent mating-type information regulator 2 homolog 1 (SIRT1) expression has been linked to cancer prognosis. However, reports evaluating the impact of SIRT1 polymorphisms on esophageal cancer (EC) risk or prognosis are limited. The present study aimed to assess the association between SIRT1 rs12778366 polymorphism and esophageal cancer. - Source: PubMed
Publication date: 2026/06/23
Bali Jagmohan SinghSambyal VasudhaMehrotra SanjanaGuleria KamleshUppal Manjit SinghManjari MriduSudan Meena - The clinical translation of nanomedicine for solid tumours remains limited despite substantial advances in biomaterial design and molecular targeting, primarily due to the physical inaccessibility of tumour tissue. Solid tumours exhibit a mechanically abnormal microenvironment characterised by extracellular matrix (ECM) densification, elevated solid stress, increased interstitial fluid pressure (IFP), and dysfunctional vasculature, which collectively establish a transport-limiting system that restricts drug penetration and promotes heterogeneous intratumoral distribution. Within this context, nanomedicine failure is best understood as a transport-limited problem in which physical constraints represent dominant, though not exclusive, determinants of therapeutic outcome. This review presents a mechanotherapeutic framework that integrates tumour mechanics with transport principles to guide biomaterial design and improve intratumoral delivery. Mechanotherapeutic strategies are categorised into three complementary approaches: (i) stiffness-modulating systems that remodel the extracellular matrix, (ii) deformable and penetration-optimised materials that navigate structural constraints, and (iii) pressure-alleviating and vessel-normalising systems that restore transport and perfusion. The framework is further extended to incorporate mechanochemical coupling through the representative reactive oxygen species (ROS), AMP-activated protein kinase (AMPK), and sirtuin 1 (SIRT1), linking mechanical stress with redox and metabolic adaptation and informing responsive biomaterial design. Integration with microdevice-enabled platforms, including microfluidic and tumour-on-chip systems, provides a quantitative and experimentally controllable platform for evaluating transport behaviour and optimising delivery strategies. Key translational challenges and future directions towards integrated and precision mechanomedicine are discussed. Collectively, this mechanotherapeutic framework provides a physically informed and experimentally actionable strategy for overcoming transport barriers and advancing the clinical translation of cancer nanomedicine. - Source: PubMed
Publication date: 2026/06/23
Singh Fathe - Methylmalonic acidemia is an inherited neurometabolic disorder characterized by accumulation of methylmalonic acid (MMA) in different tissues, particularly in the brain. As a result, patients frequently exhibit progressive neurological deterioration, accompanied by episodes of acute encephalopathy following metabolic decompensation. Astrocytes are glial cells that maintain the central nervous system homeostasis and may be important cellular targets of MMA-induced dysfunction. However, most in vitro experimental models for the study of methylmalonic acidemia are based on short-term exposure to the toxic metabolites that accumulate in patients. In this study, we used a prolonged experimental model, which has not been yet explored in the context of glial cells, focusing on the inflammatory response, glutamate metabolism, and putative signaling pathways that can contribute to understanding cellular damage observed in methylmalonic acidemia. It is emphasized that MMA is persistently elevated in the brain of the affected patients. Prolonged MMA exposure induced inflammation with significant increase in gene expression of cyclooxygenase 2, interleukin (IL)-1β and its receptor (IL1R1), and IL-6, accompanied by a decrease in IL-10 expression. MMA also increased glutamate uptake and the activity and gene expression of the enzyme glutamine synthetase, while it downregulated glial cell-derived neurotrophic factor (GDNF). The expression of NFκB, p38 MAPK, Nrf2, heme oxygenase 1, PGC-1α, and sirtuin 1 were also modulated by MMA treatment, indicating the critical role of these signaling pathways in the MMA-induced persistent gliotoxicity. Finally, it is conceivable that these changes may significantly contribute to clarify the pathogenesis of methylmalonic acidemia. - Source: PubMed
Publication date: 2026/06/23
de Souza Almeida Rômulo RodrigoBobermin Larissa DanieleSchmitz IzavianyDias Filipe Renato PereiraBezerra Caio César RamalhoRocke-Peters MarianaRezena EsterWartchow Krista MinéiaFontella Fernanda UrruthSouza Diogo OnofreWajner MoacirGonçalves Carlos-AlbertoLeipnitz GuilhianQuincozes-Santos André - Autoimmune thyroiditis (AIT) is characterized by extensive lymphocytic infiltration and progressive destruction of thyroid follicular cells (TFCs), yet the molecular mechanisms underlying persistent thyroid injury remain poorly defined. Here, methyltransferase-like 3 (METTL3) mediated N-methyladenosine (mA) modification is identified as a central driver of thyroid inflammation. METTL3 expression and mA levels were markedly increased in TFCs from AIT patients and EAT mice, and are positively associated with immune inflammation scores. Genetic or pharmacological inhibition of METTL3 suppressed the KDR (kinase insert domain receptor, also known as vascular endothelial growth factor receptor 2, VEGFR2)/VEGFA signaling loop, reduced inflammatory cytokine release and lymphocyte infiltration, restored Th17/Treg homeostasis, and alleviated thyroid injury. Mechanistically, ROS promoted METTL3 transcription through inhibition of SIRT1-dependent epigenetic repression, while METTL3-mediated m6A modification stabilized KDR mRNA in a YTHDC2-dependent manner. In turn, activated KDR established an autocrine-paracrine KDR/VEGFA amplification circuit that sustained inflammatory signaling. Together, these findings uncover the METTL3-KDR axis as a critical epitranscriptomic mechanism driving chronic thyroid inflammation and nominate it as a promising therapeutic target for AIT. - Source: PubMed
Publication date: 2026/06/23
Hu QingyiLiu HuanRen AnwenTang ZimeiTan JieYang WenMing JieHuang Tao - Cyclophosphamide (CP) has long been employed in cancer treatment as well as in therapeutic regimens for autoimmune diseases. Despite its clinical value, one of its major drawbacks is testicular damage which may be due to disruption of antioxidant defenses, amplification of inflammatory responses, and suppression of autophagy. Febuxostat is a xanthine oxidase inhibitor with promising antioxidant, anti-inflammatory, and autophagy-inducing effects. The present study investigated whether febuxostat could mitigate CP-induced testicular toxicity in a rat model. Fifty male Sprague-Dawley rats were aligned into five groups: a control group, a CP-only group, and three CP-treated groups receiving febuxostat at doses of 5, 10, or 15 mg/kg/day. Seminal fluid, blood samples, and testicular tissues were collected and analyzed through biochemical assays and pathological examinations. Febuxostat dose-dependently restored the hormonal balance, enhanced antioxidant defenses, increased sirtuin-1 levels, and modulated both NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-driven pyroptosis and mammalian target of rapamycin (mTOR)-autophagy axis in the testicular tissues of CP-treated rats compared with CP-only rats. These improvements were consistently observed in the histopathological and immunohistochemical evaluations. Owing to its antioxidant, anti-inflammatory, autophagy-promoting, and pyroptosis-modulating effects, febuxostat may show promise as a potential therapeutic option for reducing CP-related gonadal dysfunction in males. - Source: PubMed
Publication date: 2026/06/22
Atia Hanan AbdelmawgoudElariny Hemat AAbdallah Marwa HKhalifa Amany MHellal DoaaAlghubayshi AliKabel Ahmed M