Ask about this productRelated genes to: ERCC1 antibody
- Gene:
- ERCC1 NIH gene
- Name:
- ERCC excision repair 1, endonuclease non-catalytic subunit
- Previous symbol:
- -
- Synonyms:
- RAD10
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-05-23
Related products to: ERCC1 antibody
Related articles to: ERCC1 antibody
- The development of next-generation nanotheranostics is increasingly challenged by the dual imperatives of environmental sustainability and the urgent need to overcome complex biological barriers, particularly multidrug resistance (MDR) in hepatocellular carcinoma (HCC). Herein, we bridge the gap between circular economy principles and precision nanomedicine by upcycling discarded eggshell membranes (ESM) into a hierarchical metabolic therapeutic platform. Utilizing the protein fiber network of ESM as a natural biotemplate, we orchestrated the anisotropic growth of calcium carbonate (CaCO) into unique yolk-shell nanostructures (YSNs) via interfacial molecular recognition. This bioinspired architecture features a high specific surface area, enabling the efficient coloading of the chemotherapeutic cisplatin (CDDP) and ultrathin vanadium carbide (VC) MXene nanozymes, stabilized by a biotinylated carboxymethyl chitosan (Biotin-CMCS) targeting shell. Mechanistically, this "Trojan Horse" system exploits the acidic tumor microenvironment (TME) to trigger a rapid cascade of disassembly, releasing a surge of Ca ions and MXene-driven reactive oxygen species (ROS). Crucially, we demonstrate that the resulting mitochondrial calcium overload instigates a catastrophic "bioenergetic crisis," characterized by the irreversible opening of mitochondrial permeability transition pores (mPTP) and the precipitous depletion of intracellular adenosine triphosphate (ATP). This metabolic collapse effectively deactivates ATP-dependent DNA repair machineries (e.g.,poly(ADP-ribose) polymerase 1 (PARP1) and excision repair cross-complementation group 1 (ERCC1)), thereby reversing cisplatin resistance and sensitizing tumor cells to DNA damage. In vivo evaluations in HCC xenografts confirm potent tumor regression with minimal systemic toxicity, facilitated by the renal clearance of biodegradable calcium metabolites. This work presents a paradigm shift in material design, transforming biowaste into a metabolic reprogramming weapon for sustainable and effective cancer therapy. - Source: PubMed
Publication date: 2026/04/15
Shi ShupengLiu HaicongPeng QingpingNan ShenaoLiu ShuyanWei LinnaWang HaoyuWang KaiZhong XiaohongChen XinGao Wenzhe - Mutations in the Ercc1 gene, essential for DNA repair, are associated with accelerated aging and metabolic disturbances, but data on lipid composition under its deficiency remain limited. To address this gap, we analyzed the fatty acid (FA) profiles and lipids of the mevalonate pathway in mouse embryonic fibroblasts (MEFs) and in brains, livers, and kidneys of Ercc1 and wild-type (WT) mice. Ercc1 MEFs showed significantly reduced FA levels, while in brains and livers, differences vs. WT were not significant, though males tended to have lower values. Isoprenoids exhibited more pronounced changes. Squalene content was higher in Ercc1 MEFs and in female brains. Meanwhile, cholesterol levels decreased in MEFs and male brains but increased in livers. These findings indicate tissue- and sex-specific disruptions of sterol homeostasis. Notably, dolichols, recognized markers of aging, were significantly elevated in the brains and livers of Ercc1 mice, accompanied by shifts in their chain-length distribution. Only subtle sex-dependent differences were observed in the kidneys, without consistent changes in sterol, cholesterol and dolichol levels. Gene expression analysis partially supported these findings. In brains, Srd5a3 upregulation corresponded with dolichol accumulation; however, reduced Dhcr24 expression did not lower cholesterol levels. In livers, increased NgBR and Dhdds expression corresponded with higher dolichol levels. Kidneys displayed broad downregulation of mevalonate pathway genes, yet metabolite levels remained essentially unchanged. Overall, Ercc1 deficiency causes significant tissue- and sex-dependent disturbances in lipid metabolism, particularly affecting dolichol synthesis. Such alterations may contribute to the hallmarks of accelerated aging and neurodegeneration, associated with impaired DNA repair. - Source: PubMed
Publication date: 2026/04/05
Dziuban-Lech DorotaLipko AgataRobinson Andria RCzerwińska-Kostrzewska JolantaTudek BarbaraNiedernhofer Laura JSwiezewska EwaSpeina Elżbieta - - Source: PubMed
Publication date: 2026/04/07
Xia CunbingChen YangYin XindongZhu YongkangWang GaoyuanChen DexuanShen TongYang XiaojunSun HaijianZhu Hong - Recombinational repair provides an important pathway for the repair of DNA double strand breaks that arise in mitotic and meiotic cells. Homologous pairing and strand exchange leads to the formation of DNA intermediates that are linked by double Holliday junctions, and these need to be resolved prior to chromosome segregation and cell division. In mitotic cells, resolution occurs by either of two distinct pathways (i) Nucleolytic cleavage by GEN1 or SLX1-SLX4-MUS81-EME1-XPF-ERCC1 (SMX complex), or (ii) dissolution mediated by BLM-TopoIIIα-RMI1-RMI2 (BTRR complex). To facilitate the biochemical analysis of these pathways, we previously developed a novel methodology, involving DNAzyme self-cleavage, to generate 1.8-kb long DNA molecules containing dHJs. This involved the sequential annealing of precursor ssDNAs, which were first individually isolated through multiple rounds of gel purification and ethanol precipitation, but unfortunately the method was laborious and inefficient as considerable DNA losses were incurred at each step. Here, we describe a significantly improved methodology, that increases both the efficiency and yield without impacting the quality of the dHJs produced. The new method is rapid and simple, requiring only basic molecular biology expertise, and results in the formation of dHJs that make ideal substrates for the biochemical analysis of dissolution and resolution reaction in vitro. - Source: PubMed
Publication date: 2026/03/25
Shah Punatar RajveeHo Han NWest Stephen C - Non-atherosclerotic vascular aging (NAVA) contributes to cardiovascular risk through progressive arterial stiffening and endothelial dysfunction. Colchicine, best known for anti-inflammatory activity, has been proposed to protect vascular structure and function. We evaluated whether chronic colchicine mitigates NAVA in a smooth-muscle-specific ERCC1 knockout (SMC-KO) mouse model of DNA-damage-driven vascular aging. - Source: PubMed
Publication date: 2026/02/07
Mohammadi Jouabadi SoroushJüttner Annika AGolshiri KeivanAtaei Ataabadi Ehsande Boer MartineDe Vries ReneVan Veghel RichardGoos YoëlleBoon YouriMusterd-Bhaggoe UshaDuncker Dirk JMaassenVanDenBrink AntoinetteDanser A H JanBax Willem ACornel Jan HRoks Anton J M