更新于：2024-11-01

ERCC4 x ERCC1

更新于：2024-11-01

基本信息

关联

项与 ERCC4 x ERCC1 相关的药物

ERCC1-XPFinhibitors(University of Alberta)

靶点

ERCC1 x ERCC4

作用机制

ERCC1 inhibitors [+1]

在研机构

University of Alberta

原研机构

University of Alberta

在研适应症

肿瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

XPF/ERCC1 (NERx Biosciences)

靶点

ERCC1 x ERCC4

作用机制

ERCC1 modulators [+1]

在研机构

NERx Biosciences, Inc.

原研机构

NERx Biosciences, Inc.

在研适应症-

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 ERCC4 x ERCC1 相关的临床结果

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100 项与 ERCC4 x ERCC1 相关的转化医学

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0 项与 ERCC4 x ERCC1 相关的专利（医药）

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476

项与 ERCC4 x ERCC1 相关的文献（医药）

2024-09-01·International Immunopharmacology

Harmine inhibits pulmonary fibrosis through regulating DNA damage repair-related genes and activation of TP53-Gadd45α pathway

Article

作者: Liu, Jiangyun ; Zhang, Haibo ; Hu, Junping ; Zhang, Fei ; Yang, Jianhua ; Zhao, Yicong ; Wang, Jie ; Gong, Yuehong ; Pan, Meichi

BACKGROUNDHarmine has many pharmacological activities and has been found to significantly inhibit the fibrosis of keloid fibroblasts. DNA damage repair (DDR) is essential to prevent fibrosis. This study aimed to investigate the effects of harmine on pulmonary fibrosis and its underlying mechanisms.METHODSBleomycin and TGF-β1 were used to construct pulmonary fibrosis models in vivo and in vitro, then treated with harmine to explore harmine's effects in treating experimental pulmonary fibrosis and its related mechanisms. Then, RNA sequencing was applied to investigate further the crucial DDR-related genes and drug targets of harmine against pulmonary fibrosis. Finally, the expression levels of DDR-related genes were verified by real-time quantitative PCR (RT-qPCR) and western blot.RESULTSOur in vivo experiments showed that harmine treatment could improve weight loss and lung function and reduce tissue fibrosis in mice with pulmonary fibrosis. The results confirmed that harmine could inhibit the viability and migration of TGF-β1-induced MRC-5 cells, induce their apoptosis, and suppress the F-actin expression, suggesting that harmine could suppress the phenotypic transition from lung fibroblasts to lung myoblasts. In addition, RNA sequencing identified 1692 differential expressed genes (DEGs), and 10 DDR-related genes were screened as critical DDR-related genes. RT-qPCR and western blotting showed that harmine could down-regulate the expression of CHEK1, ERCC1, ERCC4, POLD1, RAD51, RPA1, TOP1, and TP53, while up-regulate FEN1, H2AX and GADD45α expression.CONCLUSIONSHarmine may inhibit pulmonary fibrosis by regulating DDR-related genes and activating the TP53-Gadd45α pathway.

2024-06-30·Chinese journal of cancer research = Chung-kuo yen cheng yen chiu

Nucleotide excision repair gene polymorphisms and hepatoblastoma susceptibility in Eastern Chinese children: A five-center case-control study.

Article

作者: Lu, Hongting ; He, Jing ; Wang, Xianqiang ; Yin, Huimin ; He, Shaohua ; Zhou, Chunlei ; Zhang, Shouhua ; Wang, Yizhen ; Zhang, Wenli

ObjectiveNucleotide excision repair (NER) plays a vital role in maintaining genome stability, and the effect of NER gene polymorphisms on hepatoblastoma susceptibility is still under investigation. This study aimed to evaluate the relationship between NER gene polymorphisms and the risk of hepatoblastoma in Eastern Chinese Han children.MethodsIn this five-center case-control study, we enrolled 966 subjects from East China (193 hepatoblastoma patients and 773 healthy controls). The TaqMan method was used to genotype 19 single nucleotide polymorphisms (SNPs) in NER pathway genes, including ERCC1, XPA, XPC, XPD, XPF, and XPG. Then, multivariate logistic regression analysis was performed, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were utilized to assess the strength of associations.ResultsThree SNPs were related to hepatoblastoma risk. XPC rs2229090 and XPD rs3810366 significantly contributed to hepatoblastoma risk according to the dominant model (adjusted OR=1.49, 95% CI=1.07-2.08, P=0.019; adjusted OR=1.66, 95% CI=1.12-2.45, P=0.012, respectively). However, XPD rs238406 conferred a significantly decreased risk of hepatoblastoma under the dominant model (adjusted OR=0.68, 95% CI=0.49-0.95; P=0.024). Stratified analysis demonstrated that these significant associations were more prominent in certain subgroups. Moreover, there was evidence of functional implications of these significant SNPs suggested by online expression quantitative trait loci (eQTLs) and splicing quantitative trait loci (sQTLs) analysis.ConclusionsIn summary, NER pathway gene polymorphisms (XPC rs2229090, XPD rs3810366, and XPD rs238406) are significantly associated with hepatoblastoma risk, and further research is required to verify these findings.

2024-05-01·Journal of Cellular Physiology

Role of c‐Fos in DNA damage repair

Review

作者: Wu, Yilun ; Yao, Haiyang ; Guo, Zimo ; Zhong, Yiming ; Wang, Xianli ; Jin, Yinpeng ; Huang, Chenxuan

Abstractc‐Fos, a member of the immediate early gene, serves as a widely used marker of neuronal activation induced by various types of brain damage. In addition, c‐Fos is believed to play a regulatory role in DNA damage repair. This paper reviews the literature on c‐Fos' involvement in the regulation of DNA damage repair and indicates that genes of the Fos family can be induced by various forms of DNA damage. In addition, cells lacking c‐Fos have difficulties in DNA repair. c‐Fos is involved in tumorigenesis and progression as a proto‐oncogene that maintains cancer cell survival, which may also be related to DNA repair. c‐Fos may impact the repair of DNA damage by regulating the expression of downstream proteins, including ATR, ERCC1, XPF, and others. Nonetheless, the underlying mechanisms necessitate further exploration.