ArticlePLoS genetics2014
The sequence-specific transcription factor c-Jun targets Cockayne syndrome protein B to regulate transcription and chromatin structure.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 36 citations in OpenAlex.
- Auranofin Potentiates Cisplatin Response in the Setting of Context-Dependent NOTCH-Associated Signaling States in Endometrial Cancer.Cancer research communications · 2026Article
- Structural basis of RECQL5-induced RNA polymerase II transcription braking and subsequent reactivation.Nature structural & molecular biology · 2025Article
- Cockayne syndrome B protein is implicated in transcription and associated chromatin dynamics in homeostatic and genotoxic conditions.Aging cell · 2025Article
- The CSB chromatin remodeler regulates PARP1- and PARP2-mediated single-strand break repair at actively transcribed DNA regions.Nucleic acids research · 2023Article
- Dynamic Interplay between Cockayne Syndrome Protein B and Poly(ADP-Ribose) Polymerase 1 during Oxidative DNA Damage Repair.Biomedicines · 2022Article
- LEO1 is a partner for Cockayne syndrome protein B (CSB) in response to transcription-blocking DNA damage.Nucleic acids research · 2021Article
- The Winged Helix Domain of CSB Regulates RNAPII Occupancy at Promoter Proximal Pause Sites.International journal of molecular sciences · 2021Article
- 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 proteins CSA and CSB maintain mitochondrial homeostasis through NADAging cell · 2020Article
- Cockayne syndrome B protein acts as an ATP-dependent processivity factor that helps RNA polymerase II overcome nucleosome barriers.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A Novel Flow Cytometric Assay to Identify Inhibitors of RBPJ-DNA Interactions.SLAS discovery : advancing life sciences R & D · 2020Article
- The SWI/SNF ATP-Dependent Chromatin Remodeling Complex in Arabidopsis Responds to Environmental Changes in Temperature-Dependent Manner.International journal of molecular sciences · 2020Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging.Nucleic acids research · 2019Article
- Poly(ADP-ribose) polymerase 1 (PARP1) promotes oxidative stress-induced association of Cockayne syndrome group B protein with chromatin.The Journal of biological chemistry · 2018Article
- Mechanistic insights into the regulation of transcription and transcription-coupled DNA repair by Cockayne syndrome protein B.Nucleic acids research · 2018Article
- NAP1L1 accelerates activation and decreases pausing to enhance nucleosome remodeling by CSB.Nucleic acids research · 2017Article
- Cockayne syndrome group A and B proteins converge on transcription-linked resolution of non-B DNA.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- ERK/c-Jun Recruits Tet1 to Induce Zta Expression and Epstein-Barr Virus Reactivation through DNA Demethylation.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cockayne syndrome is an inherited premature aging disease associated with numerous developmental and neurological defects, and mutations in the gene encoding the CSB protein account for the majority of Cockayne syndrome cases. Accumulating evidence suggests that CSB functions in transcription regulation, in addition to its roles in DNA repair, and those defects in this transcriptional activity might contribute to the clinical features of Cockayne syndrome. Transcription profiling studies have so far uncovered CSB-dependent effects on gene expression; however, the direct targets of CSB's transcriptional activity remain largely unknown. In this paper, we report the first comprehensive analysis of CSB genomic occupancy during replicative cell growth. We found that CSB occupancy sites display a high correlation to regions with epigenetic features of promoters and enhancers. Furthermore, we found that CSB occupancy is enriched at sites containing the TPA-response element. Consistent with this binding site preference, we show that CSB and the transcription factor c-Jun can be found in the same protein-DNA complex, suggesting that c-Jun can target CSB to specific genomic regions. In support of this notion, we observed decreased CSB occupancy of TPA-response elements when c-Jun levels were diminished. By modulating CSB abundance, we found that CSB can influence the expression of nearby genes and impact nucleosome positioning in the vicinity of its binding site. These results indicate that CSB can be targeted to specific genomic loci by sequence-specific transcription factors to regulate transcription and local chromatin structure. Additionally, comparison of CSB occupancy sites with the MSigDB Pathways database suggests that CSB might function in peroxisome proliferation, EGF receptor transactivation, G protein signaling and NF-κB activation, shedding new light on the possible causes and mechanisms of Cockayne syndrome.
Indexed as
Identifiers
What OpenQuestion holds
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.