ArticleCell death & disease2020
Inactivation of ribosomal protein S27-like impairs DNA interstrand cross-link repair by destabilization of FANCD2 and FANCI.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Integrative proteomics defines FANCA as a multifunctional hub linking DNA repair to translation.iScience · 2026Article
- PPP2R2C confers radioresistance in nasopharyngeal carcinoma by suppressing ferroptosis via RPS27L stabilization.Cell death & disease · 2026Article
- RPS27L Enhances Myogenesis and Muscle Mass by Targeting IGF1 Through Liquid-Liquid Phase Separation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- BCL11A deficiency protects epidermis from UVB-induced damage through promotion of autophagy.Communications biology · 2025Article
- A FANCD2 gene mutation case analysis providing potential insights into the molecular mechanisms of gastric adenocarcinoma: A case report.Oncology letters · 2025Article
- Subfunctionalized expression drives evolutionary retention of ribosomal protein paralogseLife · 2023Article
- Deregulation of ribosomal proteins in human cancers.Bioscience reports · 2021Review
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- Localization and Functional Roles of Components of the Translation Apparatus in the Eukaryotic Cell Nucleus.Cells · 2021Review
- Ribosome Biogenesis and Cancer: Overview on Ribosomal Proteins.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ribosomal protein S27-like (RPS27L), an evolutionarily conserved ribosomal protein and a direct p53 target, plays an important role in maintenance of genome integrity. We have previously reported that RPS27L regulates radiation sensitivity via the MDM2-p53 and MDM2-MRN-ATM axes. Whether and how RPS27L modulates DNA interstrand cross-link (ICL) repair is unknown. Here we identified that RPS27L binds to FANCD2 and FANCI, two Fanconi anemia (FA) proteins functioning in ICL repair pathway. Upon RPS27L knockdown, the levels of FANCD2 and FANCI are reduced due to accelerated degradation via p62-mediated autophagy-lysosome pathway, which is abrogated by chloroquine (CQ) treatment or Beclin 1 knockdown. Biologically, RPS27L knockdown suppresses FANCD2 foci formation and impairs ICL repair upon exposure to ICL-inducing agent mitomycin C (MMC) in lung cancer cells. This effect of MMC sensitization can be partially reversed by CQ treatment. Together, our study shows that RPS27L positively regulates ICL repair by binding with FANCD2 and FANCI to prevent their degradation via autophagy-lysosome system.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.