ERCC1
- Known as:
- ERCC1
- Catalog number:
- Y214009
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ERCC1
Related genes to: ERCC1
- 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
Related articles to: ERCC1
- SLX4 is a scaffold protein pivotal in genome protection mechanisms ranging from homologous recombination and interstrand cross-link (ICL) repair to mechanisms that deal with challenged DNA replication. Many of human SLX4 functions rely on its ability to interact and control the XPF-ERCC1, MUS81-EME1, and SLX1 structure-specific endonucleases. Interaction with MUS81 relies on the conserved SAP domain of SLX4. Since the same domain in yeast Slx4 orthologs does not interact with Mus81, we investigated whether human SLX4 SAP might have retained some ancestral MUS81-independent functions. We show that human SLX4 SAP binds DNA with a preference for branched structures such as Holliday junctions. We further discovered that phosphorylation of SLX4 SAP by CDK1, which promotes interaction with MUS81, inhibits DNA binding. We identified separation of function mutants that impair either DNA or MUS81 binding. Binding to MUS81 is required in response to ICL-inducing agents, methyl methanesulfonate (MMS), TOP1, and PARP inhibition. Instead, DNA binding is required in response to ICL-inducing agents and MMS but not after TOP1 or PARP inhibition. Our work indicates that phosphorylation by CDK1 acts as a regulatory switch between DNA binding and MUS81-dependent functions of SLX4, to accommodate specific DNA lesions or secondary structures. - Source: PubMed
Scaglione SarahGaillard Pierre-Henri - Despite the adoption of neoadjuvant FLOT chemotherapy as standard treatment for locally advanced gastric and gastroesophageal junction cancer, many patients fail to achieve meaningful pathological response, limiting efficacy. The aim of this study was to evaluate the impact of pharmacogenetic markers on pathological response in Russian patients receiving neoadjuvant FLOT. Thirty patients with locally advanced gastric or gastroesophageal junction adenocarcinoma received neoadjuvant FLOT followed by surgery. Polymorphisms in (rs776746), (rs10509681, rs11572080, rs1058930), (rs11615), and (rs1695) were analyzed. Favorable pathological response (TRG0-2) was observed in 23.3% of patients, including 3.3% complete responses. Most patients (76.7%) had minimal or no regression (TRG3-5). Clinical variables were not associated with response. (rs11615) showed a significant association: patients with the Wt/Wt genotype had higher odds of achieving TRG0-2 (OR = 8.889; = 0.033; 95% CI: 1.294-61.058). No associations were found for , or . Median PFS was 18.21 months in TRG3-5, while not reached in TRG0-2 ( = 0.108). No significant PFS differences by genotype were observed ( = 0.525). (rs11615) may serve as a potential pharmacogenetic marker of response to FLOT, supporting further research in personalized treatment strategies. - Source: PubMed
Publication date: 2026/05/04
Fedorinov DenisLyadov VladimirLyadova MarinaAbdullaev SherzodKachanova AnastasiaFilatova AnnaIvashchenko DmitriySychev Dmitry - Genetic susceptibility is believed to contribute to leukemia development. This study aimed to systematically evaluate the association between DNA repair gene polymorphisms, particularly xeroderma pigmentosum (XP) and excision repair cross-complementing (XRCC) genes, and leukemia risk. - Source: PubMed
Publication date: 2026/04/23
Ye HonghuiFang JinyongJin Pei - Blocking the synthesis of HBV covalently closed circular (ccc)DNA is crucial for achieving a viral cure. Previous work showed that inhibiting nucleotide excision repair (NER) reduced cccDNA levels in HBV-producing liver cells. Here, we aimed to clarify the role of NER endonucleases in addressing the flap structure on relaxed circular DNA (rcDNA) and to explore an antiviral strategy that disrupts viral replication reservoirs. - Source: PubMed
Publication date: 2026/02/28
Hung Hsu-ChinTsai Hung-WenLi Yung-TsungLiu Wen-ChunCheng Kuang-HsiungYen Chia-JuiLee Yun-PingFang Yuan-HsinChuang Cheng-HsiangWu Hui-LinChang Ting-TsungHuang Wenya - 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