ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
E2F1 coregulates cell cycle genes and chromatin components during the transition of oligodendrocyte progenitors from proliferation to differentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 74 citations in OpenAlex.
- Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation.Nature neuroscience · 2026Article
- Impaired myelination in multiple sclerosis organoids: p21 links oligodendrocyte dysfunction to disease subtype.Frontiers in cellular neuroscience · 2026Article
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- ENQUIRE automatically reconstructs, expands, and drives enrichment analysis of gene and Mesh co-occurrence networks from context-specific biomedical literature.PLoS computational biology · 2025Article
- Article
- Trametinib, an anti-tumor drug, promotes oligodendrocytes generation and myelin formation.Acta pharmacologica Sinica · 2024Article
- Histone H4 acetylation differentially modulates proliferation in adult oligodendrocyte progenitors.The Journal of cell biology · 2024Article
- DNA hypomethylation activates Cdk4/6 and Atr to induce DNA replication and cell cycle arrest to constrain liver outgrowth in zebrafish.Nucleic acids research · 2024Article
- Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2023Review
- Article
- The stability of the myelinating oligodendrocyte transcriptome is regulated by the nuclear lamina.Cell reports · 2023Article
- The epigenetic landscape of oligodendrocyte lineage cells.Annals of the New York Academy of Sciences · 2023Review
- UHRF1 overexpression promotes osteosarcoma metastasis through altered exosome production and AMPK/SEMA3E suppression.Oncogenesis · 2022Article
- Disrupted myelination network in the cingulate cortex of Parkinson's disease.IET systems biology · 2022Article
- Nests of dividing neuroblasts sustain interneuron production for the developing human brain.Science (New York, N.Y.) · 2022Article
- E2F1 Affects the Therapeutic Response to Neoadjuvant Therapy in Breast Cancer.Disease markers · 2022Article
- Transcriptional Reprogramming in Rumen Epithelium during the Developmental Transition of Pre-Ruminant to the Ruminant in Cattle.Animals : an open access journal from MDPI · 2021Article
- Oligodendrocyte progenitors as environmental biosensors.Seminars in cell & developmental biology · 2021Review
- Chromatin regulators in retinoblastoma: Biological roles and therapeutic applications.Journal of cellular physiology · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Cell cycle exit is an obligatory step for the differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating cells. A key regulator of the transition from proliferation to quiescence is the E2F/Rb pathway, whose activity is highly regulated in physiological conditions and deregulated in tumors. In this paper we report a lineage-specific decline of nuclear E2F1 during differentiation of rodent OPC into oligodendrocytes (OLs) in developing white matter tracts and in cultured cells. Using chromatin immunoprecipitation (ChIP) and deep-sequencing in mouse and rat OPCs, we identified cell cycle genes (i.e., Cdc2) and chromatin components (i.e., Hmgn1, Hmgn2), including those modulating DNA methylation (i.e., Uhrf1), as E2F1 targets. Binding of E2F1 to chromatin on the gene targets was validated and their expression assessed in developing white matter tracts and cultured OPCs. Increased expression of E2F1 gene targets was also detected in mouse gliomas (that were induced by retroviral transformation of OPCs) compared with normal brain. Together, these data identify E2F1 as a key transcription factor modulating the expression of chromatin components in OPC during the transition from proliferation to differentiation.
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.