ArticleFrontiers in molecular neuroscience2017
Neurogenic to Gliogenic Fate Transition Perturbed by Loss of HMGB2.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- MultiGATE: integrative analysis and regulatory inference in spatial multi-omics data via graph representation learning.Nature communications · 2025Article
- Longitudinal scRNA-seq analysis in mouse and human informs optimization of rapid mouse astrocyte differentiation protocols.Nature neuroscience · 2023Article
- SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development.Nature communications · 2023Article
- Stepwise fate conversion of supporting cells to sensory hair cells in the chick auditory epithelium.iScience · 2023Article
- Putative Roles of SETBP1 Dosage on the SET Oncogene to Affect Brain Development.Frontiers in neuroscience · 2022Article
- HMGA2 Promotes Brain Injury in Rats with Cerebral Infarction by Activating TLR4/NF-Mediators of inflammation · 2022Article
- Genome editing ofJournal of toxicologic pathology · 2021Article
- Oligodendroglial Epigenetics, from Lineage Specification to Activity-Dependent Myelination.Life (Basel, Switzerland) · 2021Review
- Identification of Qk as a Glial Precursor Cell Marker that Governs the Fate Specification of Neural Stem Cells to a Glial Cell Lineage.Stem cell reports · 2020Article
- FGF Signaling Directs the Cell Fate Switch from Neurons to Astrocytes in the Developing Mouse Cerebral Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A Genome Model to Explain Major Features of Neurodevelopmental Disorders in Newborns.Biomedical informatics insights · 2019Article
- A Bivalent Securinine Compound SN3-L6 Induces Neuronal Differentiation via Translational Upregulation of Neurogenic Transcription Factors.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mouse cortical development relies heavily on a delicate balance between neurogenesis and gliogenesis. The lateral ventricular zone produces different classes of excitatory pyramidal cells until just before birth, when the production of astroglia begins to prevail. Epigenetic control of this fate shift is of critical importance and chromatin regulatory elements driving neuronal or astroglial development play an vital role. Different classes of chromatin binding proteins orchestrate the transcriptional repression of neuronal-specific genes, while allowing for the activation of astrocyte-specific genes. Through proteomic analysis of embryonic neural progenitor cells (NPCs) our group had previously identified high mobility group B2 (HMGB2), a chromatin protein dynamically expressed throughout embryonic development. In the current study using cultures of perinatal NPCs from HMGB2
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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.