ReviewNucleic acids research2021
Current and emerging roles of Cockayne syndrome group B (CSB) protein.
Review in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Transcription remodeling and stalling by cisplatin-induced interstrand crosslinks.Nature chemical biology · 2026Article
- AAV-mediated gene therapy demonstrates phenotypic rescue in a mouse model of Cockayne syndrome.The Journal of clinical investigation · 2026Article
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Topology Resetting During Transcription-Coupled Nucleotide Excision Repair.International journal of molecular sciences · 2026Review
- Recognition of multimolecular G-quadruplex regulates phase separation of cockayne syndrome B.Nucleic acids research · 2026Article
- Targeting the Mitochondrial Phenotype in Cockayne Syndrome Patient Cells: From Bioenergetic Fragility to Pharmacologic Rescue.bioRxiv : the preprint server for biology · 2026Article
- Review
- Molecular basis for CSB stimulation of the SNM1A DNA repair nuclease.Research square · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- The Nucleolus: A Central Hub for Ribosome Biogenesis and Cellular Regulatory Signals.International journal of molecular sciences · 2025Review
- It Takes a Village of Chromatin Remodelers to Regulate rDNA Expression.International journal of molecular sciences · 2025Review
- Review
- The Emerging Roles of Multimolecular G-Quadruplexes in Transcriptional Regulation and Chromatin Organization.Accounts of chemical research · 2024Article
- Article
- 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
- Cognitive Decline and Other Late-Stage Neurologic Complications in Cockayne Syndrome.Neurology. Clinical practice · 2024Article
- Cockayne Syndrome Linked to Elevated R-Loops Induced by Stalled RNA Polymerase II during Transcription Elongation.Nature communications · 2024Article
- Introducing the Role of Genotoxicity in Neurodegenerative Diseases and Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cockayne syndrome (CS) is a segmental premature aging syndrome caused primarily by defects in the CSA or CSB genes. In addition to premature aging, CS patients typically exhibit microcephaly, progressive mental and sensorial retardation and cutaneous photosensitivity. Defects in the CSB gene were initially thought to primarily impair transcription-coupled nucleotide excision repair (TC-NER), predicting a relatively consistent phenotype among CS patients. In contrast, the phenotypes of CS patients are pleiotropic and variable. The latter is consistent with recent work that implicates CSB in multiple cellular systems and pathways, including DNA base excision repair, interstrand cross-link repair, transcription, chromatin remodeling, RNAPII processing, nucleolin regulation, rDNA transcription, redox homeostasis, and mitochondrial function. The discovery of additional functions for CSB could potentially explain the many clinical phenotypes of CSB patients. This review focuses on the diverse roles played by CSB in cellular pathways that enhance genome stability, providing insight into the molecular features of this complex premature aging disease.
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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.