Human Polyclonal ATG5 Ab
- Known as:
- Human Polyclonal ATG5 Antibody
- Catalog number:
- a0203
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal ATG5
Related genes to: Human Polyclonal ATG5 Ab
- Gene:
- ATG5 NIH gene
- Name:
- autophagy related 5
- Previous symbol:
- APG5L
- Synonyms:
- ASP, APG5, hAPG5
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2014-11-19
Related products to: Human Polyclonal ATG5 Ab
Related articles to: Human Polyclonal ATG5 Ab
- Epirubicin (EPI) can cause metabolic side effects, including chemotherapy-related diabetes, partly through oxidative stress that disrupts zinc (Zn) homeostasis and impairs autophagy. This study investigated the effects of EPI on Zn regulation and autophagy in the pancreas, as well as the modulatory role of N-acetylcysteine (NAC). Rats received EPI (9.6 mg/kg) by intraperitoneal injection (i.p.) followed 1 h later by NAC (50 or 300 mg/kg, i.p.). Glucose homeostasis was assessed using the Homeostatic Model Assessment (HOMA-IR), and β-cell function was assessed using HOMA-β levels. Plasma insulin levels, as well as insulin, proinsulin, beclin, autophagy-related proteins (ATG5), Microtubule-Associated Protein 1 Light Chain 3 (LC3), phosphorylated Akt (p-Akt), mechanistic target of rapamycin complex 1 (mTOR1), cleaved caspase-3, Zrt/Irt-like Protein 10 (ZIP10), and the proliferation marker Ki-67 in pancreatic tissue, were measured using commercial ELISA kits. Total oxidant status (TOS) and total antioxidant status (TAS) were measured using commercial colorimetric assay kits, and the oxidative stress index (OSI) was calculated. Zn levels in pancreatic tissue and plasma samples were measured using a colorimetric method. Morphological changes in the pancreas were assessed by hematoxylin and eosin staining. As a result, in the EPI group, oxidative stress and ZIP10 levels increased, whereas Zn levels decreased, as well as pancreatic autophagy, proliferation, and insulin synthesis increased. Oxidative stress decreased in both the EN-50 and EN-300 groups, with a more pronounced decrease in the EN-300 group. Furthermore, in the EN-300 group, pancreatic Zn, ZIP10, autophagy, and proliferation levels decreased, whereas mTOR1 levels increased. The pancreatic insulin synthesis observed in the EN-50 group was not observed in the EN-300 group. In conclusion, the increased autophagy observed in the Epi group may reflect an adaptive response to oxidative stress. The effects of NAC on oxidative stress may be dose-dependent, and high-dose NAC administration may suppress EPI-induced autophagy via mTOR1-mediated signaling. Furthermore, the relationship among Zn levels, autophagy, and insulin synthesis observed in the experimental groups may contribute to a better understanding of EPI-associated diabetogenic alterations. - Source: PubMed
Publication date: 2026/06/12
Afşar EbruEranıl Işıl - Finerenone, a novel non-steroidal mineralocorticoid receptor antagonist, has demonstrated significant efficacy in the management of myocardial infarction (MI). However, its direct cytoprotective effects on cardiomyocytes and vascular endothelial cells remain unclear. This study was performed to evaluate the cardioprotective and vasoprotective effects of finerenone following MI and to elucidate its underlying mechanisms. An in vitro oxygen-glucose deprivation (OGD) model was utilized to mimic ischemic conditions. H9C2 rat cardiomyoblasts and human umbilical vein endothelial cells were employed to assess the protective effects of finerenone. For in vivo assessment, a murine model of MI was established and treated with oral finerenone for 28 consecutive days. Cardioprotective outcomes were evaluated through electrocardiography, echocardiography, serum biochemical markers, histopathological analyses, and protein expression profiling. Finerenone significantly improved the viability of cardiomyocytes and endothelial cells subjected to OGD, reduced autophagosome accumulation by enhancing autophagosome degradation, inhibited apoptosis, and promoted endothelial cell migration and tube formation capacity. In vivo, finerenone improved cardiac function parameters, reduced serum levels of myocardial enzyme profiles and brain natriuretic peptides, decreased myocardial infarct size, enhanced left ventricular function, and alleviated myocardial inflammation, fibrosis and apoptosis. Mechanistically, finerenone downregulated the expression of ATG5 and apoptosis-related molecules in myocardial tissue, while enhancing the expression of Ang and VEGF involved in angiogenesis. Finerenone confers significant cardioprotection by inhibiting autophagy, apoptosis, and enhancing angiogenesis in both cardiomyocytes and vascular endothelial cells. These findings provide experimental evidence for the clinical utility of finerenone for secondary prevention after MI. - Source: PubMed
Publication date: 2026/06/12
Wang YebaoZhang JunyiLv FengZhang TingZhou Yafeng - The interaction between fatty acids and nanoparticles (NPs) is increasingly recognized. This study investigated how stearic acid (SA)/linolenic acid (LNA) and SiO NPs co-exposure affects mRNA abundance of efflux, autophagy, fatty acid metabolism, and synthesis genes in adult zebrafish, and Si concentrations and lipid accumulation in Caco-2 and HepG2 cells. In vivo, SA or LNA inhibited SiO NPs from inducing abcg1 expression, and SiO NPs and SA/LNA co-exposure decreased agap1 expression in intestines. In livers, SiO NPs and SA co-exposure increased abcg1 expression. SiO NPs increased autophagic gene expression (map 1lc3b, atg7, and becn1) in intestines but not in livers. In contrast, SiO NPs + LNA increased map 1lc3b and atg7 expression, and SiO NPs + SA increased atg5 and becn1 expression in livers. For fatty acid β-oxidation genes, SiO NPs increased acox1 expression but decreased pparaa expression in intestines, an effect altered by SA or LNA. In livers, SiO NPs decreased acox1, cpt1aa, and pparaa but increased pnpla2 expression, which was also changed by SA. For fatty acid synthesis genes, LNA increased acaca and fasn expression in SiO NP-exposed intestines. In livers, SiO NPs decreased acaca, fasn, and scd expression, which was increased by LNA. In vitro, LNA increased Si accumulation in SiO NP-exposed Caco-2 cells, whereas both fatty acids reduced Si levels in HepG2 cells. Lipid accumulation was enhanced in HepG2 cells exposed to LNA and SiO NPs + LNA. Overall, our findings highlighted the complex interplay between SiO NPs and fatty acids, with outcomes dependent on fatty acid structure and cell/tissue type. - Source: PubMed
Publication date: 2026/06/12
Lin WeiqiLi ShanmanNing JiaxinyuGan LuCao Yi - Oral squamous cell carcinoma (OSCC) remains a clinical challenge with limited prognostic tools. This study aimed to identify a novel autophagy-related gene signature for precise prognosis prediction and to elucidate its potential clinical utility in guiding risk stratification and personalized treatment strategies for OSCC patients. - Source: PubMed
Publication date: 2026/06/11
Zhang YinanGao HongyuFan YongjingWang DanFan ShuangshuangLi HuijieWang Shu - Psoriasis is an immune-driven dermatosis marked by keratinocyte hyperproliferation. GS-9620, a TLR7 agonist, previously mitigated EV71-triggered inflammation in mice; here we probe its anti-psoriatic potential and mechanisms. - Source: PubMed
Publication date: 2026/06/09
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