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Last update 08 May 2025

ERCC4

Last update 08 May 2025

Basic Info

Synonyms

DNA excision repair protein ERCC-4, DNA repair endonuclease XPF, DNA repair protein complementing XP-F cells

+ [7]

Introduction

Catalytic component of a structure-specific DNA repair endonuclease responsible for the 5-prime incision during DNA repair, and which is essential for nucleotide excision repair (NER) and interstrand cross-link (ICL) repair.

Drugs associated with ERCC4

ERCC1-XPFinhibitors(University of Alberta)

Target

ERCC1 x ERCC4

Mechanism

ERCC1 inhibitors [+1]

Active Org.

University of Alberta

Originator Org.

University of Alberta

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

XPF/ERCC1 (NERx Biosciences)

Target

ERCC1 x ERCC4

Mechanism

ERCC1 modulators [+1]

Active Org.

NERx Biosciences, Inc.

Originator Org.

NERx Biosciences, Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ERCC4

100 Translational Medicine associated with ERCC4

0 Patents (Medical) associated with ERCC4

941

Literatures (Medical) associated with ERCC4

01 Jun 2025·Biochemical Pharmacology

SLX4 and XPF are involved in cell migration and EMT in a cell-specific manner

Article

Author: Figuet, Léa ; Vicente, Clara ; Camus, Ninon ; Sekiou, Imane ; Beaumel, Sabine ; Duruisseaux, Michaël ; Jordheim, Lars Petter ; Dumontet, Charles ; Gimbert, Manon ; Cros-Perrial, Emeline

SLX4 and XPF are two proteins involved in DNA repair, but very little is known about their potential roles in other processes of cancer cell biology. We developed original cell models with CRISPR-Cas9-mediated knock-out of SLX4 and/or XPF using five different cell lines (A549, NCI-H1703, COLO-357, HT-29 and HEK-293 T), and performed characterization with cell biology experiments including migration assays, drug sensitivity testing, cell proliferation assessment and Western blots for relevant proteins. Results showed decreased migration of all models in HT-29 cells, of XPF-deficient COLO-357 cells and of SLX4-deficient HEK-293 T cells. Modified cell models had overall increased sensitivity to cisplatin and mitomycine C, and some models showed an increased frequency of double-stranded DNA damages. One NCI-H1703 cell model showed major karyotypic modifications, and epithelial to mesenchymal transition (EMT)-related proteins were modified in several models. Finally, knocking out one or both proteins in A549 cells had not the same impact on in vivo growth in mice. These original cell models allowed us to identify new and DNA repair-unrelated cellular roles of SLX4 and XPF in cancer cell biology. Our results should be considered within work on Nucleotide Excision Repair (NER) inhibition targeting SLX, XPF or other related proteins.

24 Apr 2025·Nature

Comprehensive interrogation of synthetic lethality in the DNA damage response

Article

Author: Schröder, Markus S ; Corn, Jacob E ; Schlapansky, Moritz F ; Kobel, Lena ; Cejka, Petr ; Fielden, John ; Lam, Simon ; Jackson, Stephen P ; Gallagher, Danielle N ; Siegner, Sebastian M ; Dello Stritto, Maria Rosaria ; Jost, Marco

AbstractThe DNA damage response (DDR) is a multifaceted network of pathways that preserves genome stability1,2. Unravelling the complementary interplay between these pathways remains a challenge3,4. Here we used CRISPR interference (CRISPRi) screening to comprehensively map the genetic interactions required for survival during normal human cell homeostasis across all core DDR genes. We captured known interactions and discovered myriad new connections that are available online. We defined the molecular mechanism of two of the strongest interactions. First, we found that WDR48 works with USP1 to restrain PCNA degradation in FEN1/LIG1-deficient cells. Second, we found that SMARCAL1 and FANCM directly unwind TA-rich DNA cruciforms, preventing catastrophic chromosome breakage by the ERCC1–ERCC4 complex. Our data yield fundamental insights into genome maintenance, provide a springboard for mechanistic investigations into new connections between DDR factors and pinpoint synthetic vulnerabilities that could be exploited in cancer therapy.

01 Mar 2025·Current Microbiology

Overexpressing Endopeptidase Inhibitor IseA Enhances Biomass and Biochemical Production of Bacillus licheniformis

Article

Author: Hu, Shiying ; Chen, Shouwen ; He, Penghui ; Asfandyar ; Zhang, Ruibin ; Zhang, Yongjia

Cell autolysis could lead to a decrease in both cell viability and the production of biochemicals, presenting one of the significant challenges during fermentation. Bacillus licheniformis, a gram-positive bacterium widely used in the production of various biologic products, also confronts the limitation caused by cell autolysis. In this study, we investigated the impact of peptidoglycan hydrolases (LytC, LytD, LytE, CwlC), endopeptidase inhibitor IseA, and prophage gene xpf on cell growth and biochemical synthesis in B. licheniformis DW2. The results showed that the deletion of xpf and overexpression of iseA could significantly increase cell survival. Then, xpf was deleted on iseA overexpressed strain P_P43UTR12iseA to construct engineered strain P_P43UTR12iseAΔxpf, which further enhanced viable cells. The results of cell autolysis showed that P_P43UTR12iseA could reduce cell autolysis significantly compared to the wild-type, but P_P43UTR12iseAΔxpf did not further decrease cell autolysis. Furthermore, the production of bacitracin was 792.23 U/mL in the iseA overexpressed strain, which increased by 13.82% compared with the wild-type, but P_P43UTR12iseAΔxpf did not further increase bacitracin production. Through detecting intracellular metabolites, we observed that iseA overexpression did not affect intracellular metabolism, but the precursors of bacitracin synthesis in P_P43UTR12iseAΔxpf were lower than that of wild-type and P_P43UTR12iseA. Finally, we found that the overexpression of iseA could also significantly improve the production of γ-PGA. In general, the overexpression of iseA could enhance the biomass and cell survival by reducing cell lysis without affecting the intracellular metabolites, which provided a potential strategy to improve production of biochemical.

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ERCC4

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