ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Ascl1/Mash1 promotes brain oligodendrogenesis during myelination and remyelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.
- Unraveling the mystery of white matter in depression: A translational perspective on recent advances.Brain and behavior · 2022Pooled it
- Ascl1 promotes OPC specification across species and central nervous system regions and its gliogenic function is regulated by phosphorylation.Developmental biology · 2026Article
- Impaired Complex I dysregulates neural/glial precursors and corpus callosum development revealing postnatal defects in Leigh syndrome mice.EMBO molecular medicine · 2026Article
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- The chemotherapy agent doxorubicin induces CNS expression of Ascl1, a regulator of adult neurogenesis and differentiation.Scientific reports · 2025Article
- Topological identification and interpretation for single-cell epigenetic regulation elucidation in multi-tasks using scAGDE.Nature communications · 2025Article
- Enhancer Dynamics and Spatial Organization Drive Anatomically Restricted Cellular States in the Human Spinal Cord.bioRxiv : the preprint server for biology · 2025Article
- Integrated multimodal cell atlas of Alzheimer's disease.Nature neuroscience · 2024Article
- Epigenetic Insights into Autism Spectrum Disorder: DNA Methylation Levels ofClinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024Article
- Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration.Nature communications · 2024Article
- Pharmacogenomic screening identifies and repurposes leucovorin and dyclonine as pro-oligodendrogenic compounds in brain repair.Nature communications · 2024Article
- A New Acquaintance of Oligodendrocyte Precursor Cells in the Central Nervous System.Neuroscience bulletin · 2024Review
- Using a comprehensive atlas and predictive models to reveal the complexity and evolution of brain-active regulatory elements.Science advances · 2024Article
- Single-cell approaches define two groups of mammalian oligodendrocyte precursor cells and their evolution over developmental time.Stem cell reports · 2024Article
- Interaction between Oligodendrocytes and Interneurons in Brain Development and Related Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- Unveiling the fate and potential neuroprotective role of neural stem/progenitor cells in multiple sclerosis.Frontiers in neurology · 2024Review
- Potential of Nano-Engineered Stem Cells in the Treatment of Multiple Sclerosis: A Comprehensive Review.Cellular and molecular neurobiology · 2023Review
- Notch Signaling Plays a Dual Role in Regulating the Neuron-to-Oligodendrocyte Switch in the Developing Dorsal Forebrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Distinct requirements for Tcf3 and Tcf12 during oligodendrocyte development in the mouse telencephalon.Neural development · 2023Article
- The epigenetic landscape of oligodendrocyte lineage cells.Annals of the New York Academy of Sciences · 2023Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
Oligodendrocytes are the myelin-forming cells of the CNS. They differentiate from oligodendrocyte precursor cells (OPCs) that are produced from progenitors throughout life but more actively during the neonatal period and in response to demyelinating insults. An accurate regulation of oligodendrogenesis is required to generate oligodendrocytes during these developmental or repair processes. We hypothesized that this regulation implicates transcription factors, which are expressed by OPCs and/or their progenitors. Ascl1/Mash1 is a proneural transcription factor previously implicated in embryonic oligodendrogenesis and operating in genetic interaction with Olig2, an essential transcriptional regulator in oligodendrocyte development. Herein, we have investigated the contribution of Ascl1 to oligodendrocyte development and remyelination in the postnatal cortex. During the neonatal period, Ascl1 expression was detected in progenitors of the cortical subventricular zone and in cortical OPCs. Different genetic approaches to delete Ascl1 in cortical progenitors or OPCs reduced neonatal oligodendrogenesis, showing that Ascl1 positively regulated both OPC specification from subventricular zone progenitors as well as the balance between OPC differentiation and proliferation. Examination of remyelination processes, both in the mouse model for focal demyelination of the corpus callosum and in multiple sclerosis lesions in humans, indicated that Ascl1 activity was upregulated along with increased oligodendrogenesis observed in remyelinating lesions. Additional genetic evidence indicated that remyelinating oligodendrocytes derived from Ascl1(+) progenitors/OPCs and that Ascl1 was required for proper remyelination. Together, our results show that Ascl1 function modulates multiple steps of OPC development in the postnatal brain and in response to demyelinating insults.
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.