ArticleCell death & disease2014
The cockayne syndrome B protein is essential for neuronal differentiation and neuritogenesis.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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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.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- A Truncating Variant in theGenetics research · 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
- HiPSC-derived 3D neural models reveal neurodevelopmental pathomechanisms of the Cockayne Syndrome B.Cellular and molecular life sciences : CMLS · 2024Article
- Electromagnetic Cellularized Patch with Wirelessly Electrical Stimulation for Promoting Neuronal Differentiation and Spinal Cord Injury Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Homocysteine impedes neurite outgrowth recovery after intracerebral haemorrhage by downregulating pCAMK2A.Stroke and vascular neurology · 2023Article
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
- Neurogenesis in aging and age-related neurodegenerative diseases.Ageing research reviews · 2022Review
- The Role of Transposable Elements of the Human Genome in Neuronal Function and Pathology.International journal of molecular sciences · 2022Review
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- BAZ1B the Protean Protein.Genes · 2021Review
- The Winged Helix Domain of CSB Regulates RNAPII Occupancy at Promoter Proximal Pause Sites.International journal of molecular sciences · 2021Article
- Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction.Protein & cell · 2020Article
- Nucleotide excision repair genes shaping embryonic development.Open biology · 2019Review
- Mechanistic insights into the regulation of transcription and transcription-coupled DNA repair by Cockayne syndrome protein B.Nucleic acids research · 2018Article
- The Cellular Response to Transcription-Blocking DNA Damage.Trends in biochemical sciences · 2018Review
- Cockayne syndrome-derived neurons display reduced synapse density and altered neural network synchrony.Human molecular genetics · 2016Article
- Pharmacological Bypass of Cockayne Syndrome B Function in Neuronal Differentiation.Cell reports · 2016Article
- Diagnostics of Primary Immunodeficiencies through Next-Generation Sequencing.Frontiers in immunology · 2016Article
- Photosensitive human syndromes.Mutation research · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Cockayne syndrome (CS) is a progressive developmental and neurodegenerative disorder resulting in premature death at childhood and cells derived from CS patients display DNA repair and transcriptional defects. CS is caused by mutations in csa and csb genes, and patients with csb mutation are more prevalent. A hallmark feature of CSB patients is neurodegeneration but the precise molecular cause for this defect remains enigmatic. Further, it is not clear whether the neurodegenerative condition is due to loss of CSB-mediated functions in adult neurogenesis. In this study, we examined the role of CSB in neurogenesis by using the human neural progenitor cells that have self-renewal and differentiation capabilities. In this model system, stable CSB knockdown dramatically reduced the differentiation potential of human neural progenitor cells revealing a key role for CSB in neurogenesis. Neurite outgrowth, a characteristic feature of differentiated neurons, was also greatly abolished in CSB-suppressed cells. In corroboration with this, expression of MAP2 (microtubule-associated protein 2), a crucial player in neuritogenesis, was also impaired in CSB-suppressed cells. Consistent with reduced MAP2 expression in CSB-depleted neural cells, tandem affinity purification and chromatin immunoprecipitation studies revealed a potential role for CSB in the assembly of transcription complex on MAP2 promoter. Altogether, our data led us to conclude that CSB has a crucial role in coordinated regulation of transcription and chromatin remodeling activities that are required during neurogenesis.
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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.