ATG5 Chicken Polyclonal Antibody
- Known as:
- ATG5 Chicken Polyclonal Antibody
- Catalog number:
- AUT-5031
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ATG5 Chicken Polyclonal Antibody
Related genes to: ATG5 Chicken Polyclonal Antibody
- 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: ATG5 Chicken Polyclonal Antibody
Related articles to: ATG5 Chicken Polyclonal Antibody
- Hepatocellular carcinoma (HCC) remains a therapeutic challenge due to late-stage diagnosis and suboptimal response to standard therapies. Resveratrol, a plant-derived polyphenol, suppresses proliferation of HCC cells by inducing apoptosis and autophagy. However, the regulatory mechanism that integrates these two processes is poorly understood. This study aimed to elucidate how resveratrol coordinately regulates apoptosis and autophagy in HCC cells. Using integrated network pharmacology and QIAGEN Ingenuity Pathway Analysis (IPA), was predicted as the central hub target gene of resveratrol in HCC, where it coordinated both apoptosis and autophagy. Molecular docking and molecular dynamics simulation confirmed direct and stable binding of resveratrol to p53 protein. Functional validation revealed that resveratrol significantly ( < 0.01) inhibited the viability of p53-wild-type HepG2 cells, accompanied by mRNA upregulation of pro-apoptotic and autophagy-related genes (, , , 5), with concordant changes at the protein level (upregulated Bax and ATG5 proteins, increased ratios of Bax/Bcl-2, cleaved-Caspase 9/Caspase 9, cleaved-Caspase 3/Caspase 3, and LC3B-II/I, decreased p62 protein). These effects were strictly p53-dependent, as they were absent in p53-null Hep3B cells and significantly ( < 0.05) attenuated upon pharmacological inhibition of p53 in HepG2 cells. Mechanistically, resveratrol activated p53 not by increasing its protein level but by enhancing its acetylation at Lysine 382. This study established p53 acetylation as a critical switch through which resveratrol coordinately induced apoptosis and autophagy. These findings provide a mechanistic framework for anti-HCC effect of resveratrol and underscore the therapeutic relevance of p53 activation pathways in HCC. - Source: PubMed
Publication date: 2026/04/30
Zhang HuiZhang HuidongLi WeiZhang HongXu YangLiu WenBao LiyaZhou SiyuZhang XiaoyuLi Jiao - : The aim of this study is to investigate the relationship between the expression levels of autophagy-related genes (SQSTM1, Beclin1, Atg5, and Atg7) in diffuse astrocytic tumors and clinicopathological parameters, including tumor grade, IDH mutation status, and survival outcomes. A total of 150 histopathologically confirmed diffuse astrocytic tumor cases were retrospectively analyzed. Clinical data were extracted from patient records. Gene expression levels were determined using qRT-PCR and evaluated by the 2 method, where lower ΔCt values indicate higher gene expression. IDH1 R132H mutation status was evaluated by immunohistochemistry. No statistically significant differences were observed in the expression levels of SQSTM1, Beclin1, Atg5, and Atg7 across WHO tumor grades ( > 0.05). However, when analyzed by IDH status, IDH-mutant tumors exhibited significantly higher gene expression levels (demonstrated by lower ΔCt values) of Beclin1 ( = 0.046) and Atg5 ( = 0.027) compared to IDH wild-type tumors. In multivariate Cox regression analysis, age and WHO tumor grades were confirmed as independent prognostic factors. Crucially, higher SQSTM1 expression independently predicted worse clinical outcomes, specifically poorer overall survival (OS) ( = 0.004) and shorter progression-free survival (PFS) ( = 0.031). Additionally, elevated Beclin1 expression was identified as an independent predictor of worse OS ( = 0.023). : This study demonstrates that increased expression of autophagy-related genes, particularly SQSTM1 and Beclin1, serves as a robust indicator of poor prognosis and shorter survival times in diffuse astrocytic tumors. Furthermore, the elevated expression of Beclin1 and Atg5 in IDH-mutant cases highlights a complex metabolic interplay that warrants further investigation as potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/10
Kiraz İlkerTopel GözdeAydın Veli KaanCivlan SerkanDere Ümit AkınCoşkun Mehmet ErdalYalçın NagihanLengerova GerganaBozhkova MartinaPetrov SteliyanKöseler Aylin - Kölliker's organ (KO) support cells undergo orderly, time-dependent degeneration that is essential for auditory development and is accompanied by precisely regulated autophagic activity; however, the molecular hierarchy linking autophagy to this remodeling remains obscure. This study aimed to elucidate the regulatory mechanisms connecting autophagic flux to lysosomal biogenesis and auditory function during cochlear development. - Source: PubMed
Publication date: 2026/04/01
Chen PenghuiZhang JifangWang YingChen Jiarui - The increasing contamination of aquatic ecosystems by agrochemicals and pharmaceuticals, such as abamectin (ABA), poses significant risks to fish and human health through bioaccumulation. Thereby, in the current study, largemouth bass (Micropterus salmoides) were chronically exposed to 0.012 mg/L of ABA for six weeks. Concurrently, dietary supplementation with curcumin (CUR) at 50, 100, and 200 mg/kg was administered to evaluate its protective effects against ABA-induced toxicity. ABA significantly decreased growth performance, while inducing severe behavioral alterations and cardiac damage, including necrosis, hemorrhage, and inflammatory infiltration. It triggered oxidative stress by decreasing antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), increasing inducible nitric oxide synthase (iNOS) and malondialdehyde (MDA), and disruption of nrf2, keap 1, ho-1, and nqo1. ABA-induced immune dysfunction and inflammation which were linked to NLRP3 inflammasome stimulation, demonstrated as enhanced alkaline phosphatase (AKP), acid phosphatase (ACP) and altered transcription and translation of il-10, il-1β, tgf-β1, tnf-α, asc, caspase1, nlrp3, and nf-κb. It caused apoptosis by dysregulating gene and protein level of fas, p53, bcl2, bax, and caspases. It disrupted autophagic flux by inhibiting mTOR signaling, resulting in increased expression of lc3ii, p62 and atg5; and decreased akt and mtor level. ABA residues were detected in heart tissues (P < 0.01), and total hazard quotient (THQ) indicated potential human health risks due to bioaccumulation. Integrated biomarker response (IBR) analysis and molecular docking further confirmed the exposure risk of ABA. However, CUR co-treatment effectively attenuated these toxic effects and molecular interactions. Collectively, it highlighted the possible risks for human health, emphasizing its toxicological impact whereas protective role of CUR in mitigating ABA-induced cardiotoxicity suggests a promising strategy for reducing pesticide-related health hazards in aquaculture and environmental toxicology. - Source: PubMed
Publication date: 2025/07/09
Tahir RabiaSong KaigeLuo WeizheShrestha AbhimanyuHu GuojunHuang ZihanHu YifanYan HanLiu QiaoZhao LiulanYang Song - The kappa class of glutathione S-transferases 1 (GSTK1) is a vital regulatory factor in metabolic diseases. This study was conducted to investigate the regulatory effects of GSTK1 on renal ectopic fat deposition (EFD) and lipotoxic injury in diabetic nephropathy (DN) . - Source: PubMed
Publication date: 2026/04/30
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