ArticleProceedings of the National Academy of Sciences of the United States of America2010
The RNF8/RNF168 ubiquitin ligase cascade facilitates class switch recombination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 81 citations in OpenAlex.
- Epigenetic regulation of humoral immunity: molecular mechanisms, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Riddle syndrome with RNF168 mutation in first Asian family cluster exhibiting pulmonary fibrosis and achalasia.Journal of human genetics · 2026Article
- Replication of 10 novel loci involved in human plasma protein N-glycosylation using MALDI-MS and UHPLC-FD data.Glycobiology · 2026Article
- Estrogen influences class-switched memory B cell frequency only in humans with two X chromosomes.The Journal of experimental medicine · 2025Article
- KRT80, Regulated by RNF8-Mediated Ubiquitination, Contributes to Glucose Metabolic Reprogramming and Progression of Glioblastoma.Neurochemical research · 2025Article
- Review
- Intercellular Epigenomic Signalling via Extracellular Vesicles During B Cell Maturation.Journal of extracellular vesicles · 2025Article
- Cell-Penetrating Peptide-Mediated Biomolecule Transportation in Artificial Lipid Vesicles and Living Cells.Molecules (Basel, Switzerland) · 2024Review
- Proteomic Alteration in the Progression of Multiple Myeloma: A Comprehensive Review.Diagnostics (Basel, Switzerland) · 2023Review
- Article
- Neurodevelopmental Disorders (NDD) Caused by Genomic Alterations of the Ubiquitin-Proteasome System (UPS): the Possible Contribution of Immune Dysregulation to Disease Pathogenesis.Frontiers in molecular neuroscience · 2021Review
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- Ubiquitination and Ubiquitin-Like Modifications in Multiple Myeloma: Biology and Therapy.Cancers · 2020Review
- RNF8 has both KU-dependent and independent roles in chromosomal break repair.Nucleic acids research · 2020Article
- RNF168 facilitates proliferation and invasion of esophageal carcinoma, possibly via stabilizing STAT1.Journal of cellular and molecular medicine · 2019Article
- RNF168 facilitates oestrogen receptor ɑ transcription and drives breast cancer proliferation.Journal of cellular and molecular medicine · 2018Article
- L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage.Nature cell biology · 2018Article
- A Comprehensive Atlas of E3 Ubiquitin Ligase Mutations in Neurological Disorders.Frontiers in genetics · 2018Review
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
An effective immune response requires B cells to produce several classes of antibodies through the process of class switch recombination (CSR). Activation-induced cytidine deaminase initiates CSR by deaminating deoxycytidines at switch regions within the Ig locus. This activity leads to double-stranded DNA break formation at the donor and recipient switch regions that are subsequently synapsed and ligated in a 53BP1-dependent process that remains poorly understood. The DNA damage response E3 ubiquitin ligases RNF8 and RNF168 were recently shown to facilitate recruitment of 53BP1 to sites of DNA damage. Here we show that the ubiquitination pathway mediated by RNF8 and RNF168 plays an integral part in CSR. Using the CH12F3-2 mouse B cell line that undergoes CSR to IgA at high rates, we demonstrate that knockdown of RNF8, RNF168, and 53BP1 leads to a significant decrease in CSR. We also show that 53BP1-deficient CH12F3-2 cells are protected from apoptosis mediated by the MDM2 inhibitor Nutlin-3. In contrast, deficiency in either E3 ubiquitin ligase does not protect cells from Nutlin-3-mediated apoptosis, indicating that RNF8 and RNF168 do not regulate all functions of 53BP1.
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Registered trials
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.