Ask about this productRelated genes to: PARP10 Blocking Peptide
- Gene:
- PARP10 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 10
- Previous symbol:
- -
- Synonyms:
- FLJ14464
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-25
- Date modifiied:
- 2018-07-03
Related products to: PARP10 Blocking Peptide
Related articles to: PARP10 Blocking Peptide
- The age-related decline in liver regenerative capacity worsens outcomes for elderly patients with liver disease or undergoing liver surgery, and therapeutic options are limited. The RNA modification N4-acetylcytidine (ac4C), catalyzed by N-acetyltransferase 10 (Nat10), is implicated in regeneration; however, its role in the aged liver remains unknown. - Source: PubMed
Publication date: 2026/06/18
You QiangXiao CuicuiChen HaoqiZhang GongmingZhang FengWu ZhengqiLiu YasongZhang JiebinChen HaitianXiao JiaqiChen WenjieYao JiaZhang YingcaiLi HuaLi HuiYang YangLi RongZheng Jun - Cancer remains a leading cause of death worldwide, constrained by limitations of current therapies, such as systemic toxicity, narrow therapeutic windows, and acquired drug resistance, highlighting the urgent need for novel agents. This study aimed to evaluate the antitumor efficacy of parimifasor and elucidate its molecular mechanism through transcriptomic profiling. - Source: PubMed
Publication date: 2026/04/27
Li KaiSun MinshanDu RuijuanWang QianBian BoZhang YutianBian Hua - Pancreatic cancer remains one of the most lethal malignancies, characterised by aggressive progression, metabolic adaptation, and resistance to therapy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical mechanism influencing tumour survival and therapeutic response. However, the role of ferroptosis suppressor genes (FSGs) in pancreatic cancer remains incompletely understood. In this study, FSGs were systematically retrieved from FerrDb V2 and subjected to multi-step filtering to identify a curated set of 196 protein-coding genes. Genomic alteration analysis using cBioPortal across 21 pancreatic cancer studies (n = 5189 samples) identified seven recurrently altered genes (TP53, HSF1, PARP10, ZFP36, SIRT2, ECH1, and ENPP2) with alteration frequencies ≥ 3%. Co-occurrence analysis revealed predominantly cooperative alteration patterns among these genes, suggesting functional complementarity. Survival analysis demonstrated that alterations in FSGs were significantly associated with reduced overall survival in pancreatic cancer, with several genes (ECH1, ZFP36, SIRT2, and ENPP2) showing particularly strong adverse prognostic effects. In contrast, no significant survival associations were observed in oesophageal and gastric cancers, indicating a tumour-specific dependency on ferroptosis-related mechanisms. KEGG pathway enrichment analysis of the broader FSG set revealed significant involvement in pathways related to metabolic regulation (AMPK-mTOR signalling), autophagy, hypoxia response (HIF-1 signalling), and oncogenic signalling (PI3K-Akt pathway). Integration of these findings suggests that ferroptosis suppressor genes contribute to pancreatic cancer progression by promoting metabolic adaptation and resistance to oxidative stress. In conclusion, this study identifies key ferroptosis suppressor genes with prognostic relevance in pancreatic cancer and highlights their integration within critical metabolic and stress-response pathways. The tumour-specific nature of these associations underscores the importance of biological context and supports the potential of FSGs as prognostic biomarkers and potential therapeutic targets in ferroptosis-based strategies. - Source: PubMed
Publication date: 2026/06/10
Singh Nitin KumarSingh ManinderHusain AdilAlnajjar Lina IAhmad FirozMishra Siddhartha KumarAlshamamri NawafSaeed MohdRab Safia ObaidurGupta Varsha - The increasing incidence of diabetic foot ulcer (DFU) and growing recognition of environmental pollutants have highlighted polyethylene terephthalate microplastics (PET-MP) as a potential metabolic disease trigger. However, the molecular mechanisms linking PET-MP to DFU remain unclear. This study employed integrated network toxicology and bioinformatics to decipher these mechanisms. PET-MP toxicity targets were screened using SwissTargetPrediction and ChEMBL, and DFU-related differentially expressed genes were obtained from GSE199939 and GSE134431. Functional analysis of overlapping genes included gene ontology, Kyoto encyclopedia of genes and genomes, gene set variation analysis, and protein-protein interaction network analysis. Machine learning models (least absolute shrinkage and selection operator, random forest, and support vector machine-recursive feature elimination) and SHapley Additive exPlanations analysis identified key genes, validated via nomogram, molecular dynamics simulation, and molecular docking. From 6723 DFU-related differentially expressed genes, 53 overlapping genes were identified. Functional analysis highlighted pathways including apoptosis, advanced glycation end product-receptor for advanced glycation end-product signaling, arachidonic acid metabolism, and nicotinamide adenine dinucleotide poly-ADP-ribosyltransferase activity. Machine learning and SHapley Additive exPlanations analysis identified PARP10 and PFKFB4 as key genes. Molecular docking revealed moderate binding affinities (Vina scores: -6.8 and -5.6). Molecular dynamics simulations confirmed conformational stability. PET-MP may exacerbate DFU by disrupting DNA damage repair, enhancing oxidative stress, and impairing glucose metabolism. These in silico findings identify PARP10 and PFKFB4 as potential candidate genes associated with PET-MP-related pathways in DFU, warranting further experimental validation. - Source: PubMed
Li DongxiaoMa ZhanhuaLi ZunwangFu ZhihongGuo HuiChen Zhaojun - ADP-ribosylation (ADPr) is a regulatory post-translational modification targeting nine amino acid residues, but glutamate/aspartate-linked ADPr (Glu/Asp-ADPr) is labile and remains challenging to detect using conventional mass spectrometry (MS)-based workflows. Using synthetic peptides, we show that ester-linked Glu/Asp-ADPr is lost under alkaline conditions, elevated temperatures, and by hydrolysis via wildtype Af1521. We developed an acidic enrichment workflow incorporating an Af1521 mutant that preserves Glu/Asp-ADPr, enabling site-specific, system-wide MS analysis. In cytokine-stimulated A549 and HeLa cells, we identified >600 Glu/Asp- and >200 Cys-ADPr sites. Glu/Asp-ADPr marks cytoplasmic, immune-related protein networks, contrasting with nuclear Ser-ADPr. Quantitative profiling revealed reproducible, cell type- and treatment-specific patterns. PARP10-mediated Glu/Asp ADPr of ubiquitin indicates direct crosstalk with ubiquitin signaling pathways. Interferon treatments revealed conserved antiviral PARP networks extensively modified on Glu/Asp residues. Together, our work establishes a robust MS-based workflow and provides a resource of site-specific ADPr events, revealing residue-specific ADPr in innate immune signaling. - Source: PubMed
Publication date: 2026/05/27
Buch-Larsen Sara CHendriks Ivo ATashiro KyutoElsborg Jonas DVakhrushev Sergey YOlsen Jesper VLüscher BernhardLiszczak GlenAhel IvanNielsen Michael L