ArticleCell cycle (Georgetown, Tex.)2011
CSA and CSB proteins interact with p53 and regulate its Mdm2-dependent ubiquitination.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- Targeting p53 in Cancer: Functional States, Therapeutic Strategies, and Clinical Progress.Cancers · 2026Review
- Repurposing Alkylating Agents in Melanoma via ERCC8 Silencing: A Novel Therapeutic Strategy.Cancers · 2026Article
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence.Aging cell · 2025Article
- Perspectives in the investigation of Cockayne syndrome group B neurological disease: the utility of patient-derived brain organoid models.Journal of Zhejiang University. Science. B · 2024Review
- Article
- Genetics behind Cerebral Disease with Ocular Comorbidity: Finding Parallels between the Brain and Eye Molecular Pathology.International journal of molecular sciences · 2022Review
- Neurogenesis in aging and age-related neurodegenerative diseases.Ageing research reviews · 2022Review
- CSA Antisense Targeting Enhances Anticancer Drug Sensitivity in Breast Cancer Cells, including the Triple-Negative Subtype.Cancers · 2022Article
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- Neuroblastoma Cells Depend on CSB for Faithful Execution of Cytokinesis and Survival.International journal of molecular sciences · 2021Article
- LEO1 is a partner for Cockayne syndrome protein B (CSB) in response to transcription-blocking DNA damage.Nucleic acids research · 2021Article
- Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- The Cockayne syndrome group A and B proteins are part of a ubiquitin-proteasome degradation complex regulating cell division.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cockayne syndrome group A and B proteins function in rRNA transcription through nucleolin regulation.Nucleic acids research · 2020Article
- CSB promoter downregulation via histone H3 hypoacetylation is an early determinant of replicative senescence.Nature communications · 2019Article
- Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019Article
- Design and characterization of chionodracine-derived antimicrobial peptides with enhanced activity against drug-resistant human pathogens.RSC advances · 2018Article
- Regulation of Apoptosis During Porcine Circovirus Type 2 Infection.Frontiers in microbiology · 2018Review
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Authors and funding
10 authors at 6 institutions in 6 countries.
Funding
Abstract
Mutations in Cockayne syndrome (CS) A and B genes (CSA and CSB) result in a rare genetic disease that affects the development and homeostasis of a wide range of tissues and organs. We previously correlated the degenerative phenotype of patients to the enhanced apoptotic response, exhibited by CS cells, which is associated with the exceptional induction of p53 protein, upon a variety of stress stimuli. Here we showed that the elevated and persistent levels of p53 displayed by CS cells are due to the insufficient ubiquitination of the p53 protein. We further demonstrated that CSA and CSB proteins associate in a unique complex with p53 and Mdm2; this interaction greatly stimulates the ubiquitination of p53 in an Mdm2-dependent manner. Tandem affinity purification and immunoprecipitations combined with mass spectrometry studies indicate that CSA and CSB associate within a Cullin Ring Ubiquitin Ligase complex responsible, under certain circumstances, for p53 ubiquitination. This study identifies CSA and CSB as the key elements of a regulatory mechanism that equilibrate beneficial and detrimental effects of p53 activity upon cellular stress. The deregulation of p53, in absence of either of the CS proteins, can potentially explain the early onset degeneration of tissues and organs observed in CS patients.
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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.