ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Abnormal development of forebrain midline glia and commissural projections in Nfia knock-out mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
What it found
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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
115 citing papers in PubMed, 220 citations in OpenAlex.
- Loss of Zmiz1 in Mice Leads to Impaired Cortical Development and Autistic-Like Behaviors.Biological psychiatry · 2026Article
- Structural basis for genome-wide site-specific DNA recognition by Nuclear Factor IA.Nature communications · 2025Article
- An evolutionarily conserved role for CTNNB1/β-CATENIN in regulating the development of the corpus callosum.iScience · 2025Article
- Spinal motor neuron development and metabolism are transcriptionally regulated by nuclear factor IA.Science advances · 2025Article
- Generation of human induced pluripotent stem cell lines derived from a patient carrying an intragenic deletion in the NFIA gene.Human cell · 2025Article
- Topological identification and interpretation for single-cell epigenetic regulation elucidation in multi-tasks using scAGDE.Nature communications · 2025Article
- Analysis of downstream targets of PAX6 and LHX2, fundamental regulators of the developing mammalian neocortex.Journal of biosciences · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Developmental DNA demethylation is a determinant of neural stem cell identity and gliogenic competence.Science advances · 2024Article
- Alternative splicing of a chromatin modifier alters the transcriptional regulatory programs of stem cell maintenance and neuronal differentiation.Cell stem cell · 2024Article
- Temporal-spatial Generation of Astrocytes in the Developing Diencephalon.Neuroscience bulletin · 2024Article
- Review
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- The NFIB/CARM1 partnership is a driver in preclinical models of small cell lung cancer.Nature communications · 2023Article
- Brain plasticity following corpus callosum agenesis or loss: a review of the Probst bundles.Frontiers in neuroanatomy · 2023Review
- CaCell death & disease · 2022Article
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- Human transcription factor protein interaction networks.Nature communications · 2022Article
- The Relationship between Expression of Nuclear Factor I and the Progressive Occurrence of Diabetic Retinopathy.Computational and mathematical methods in medicine · 2022Article
- Nuclear factor I-C disrupts cellular homeostasis between autophagy and apoptosis via miR-200b-Ambra1 in neural tube defects.Cell death & disease · 2021Article
55 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
Nuclear factor I (NFI) genes are expressed in multiple organs throughout development (Chaudhry et al., 1997; for review, see Gronostajski, 2000). All four NFI genes are expressed in embryonic mouse brain, with Nfia, Nfib, and Nfix being expressed highly in developing cortex (Chaudhry et al., 1997). Disruption of the Nfia gene causes agenesis of the corpus callosum (ACC), hydrocephalus, and reduced GFAP expression (das Neves et al., 1999). Three midline structures, the glial wedge, glia within the indusium griseum, and the glial sling are involved in development of the corpus callosum (Silver et al., 1982; Silver and Ogawa, 1983; Shu and Richards, 2001). Because Nfia(-)/- mice show glial abnormalities and ACC, we asked whether defects in midline glial structures occur in Nfia(-)/- mice. NFI-A protein is expressed in all three midline populations. In Nfia(-)/-, mice sling cells are generated but migrate abnormally into the septum and do not form a sling. Glia within the indusium griseum and the glial wedge are greatly reduced or absent and consequently Slit2 expression is also reduced. Although callosal axons approach the midline, they fail to cross and extend aberrantly into the septum. The hippocampal commissure is absent or reduced, whereas the ipsilaterally projecting perforating axons (Hankin and Silver, 1988; Shu et al., 2001) appear relatively normal. These results support an essential role for midline glia in callosum development and a role for Nfia in the formation of midline glial structures.
Indexed as
Identifiers
12514217PMC6742120W2117344609What 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.