ArticleCell reports2019
Chromatin Decondensation by FOXP2 Promotes Human Neuron Maturation and Expression of Neurodevelopmental Disease Genes.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 64 citations in OpenAlex.
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- Prenatal maternal immune activation triggers lasting cell-specific transcriptomic dysregulation in the amygdala of primate offspring.Molecular psychiatry · 2026Article
- Ancient regulatory evolution shapes individual language abilities in present-day humans.Science advances · 2026Article
- Nuclear Factor I-B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ancient regulatory evolution shapes individual language abilities in present-day humans.bioRxiv : the preprint server for biology · 2026Article
- Postpartum Psychosis: could genetic vulnerability to insomnia or short sleep duration be protective?Translational psychiatry · 2026Article
- Temporal Transcriptional Regulation of Human Neuronal Differentiation via Forward Programming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cerebellar organoids model cell type-specific FOXP2 expression during human cerebellar development.Disease models & mechanisms · 2025Article
- Spinal motor neuron development and metabolism are transcriptionally regulated by nuclear factor IA.Science advances · 2025Article
- Temporal control of progenitor competence shapes maturation in GABAergic neuron development in mice.Nature neuroscience · 2025Article
- Abnormal development of gastrointestinal system of homozygous Foxp2(R552H)-mutated mice.Communications biology · 2025Article
- A novel deep learning framework with dynamic tokenization for identifying chromatin interactions along with motif importance investigation.Briefings in bioinformatics · 2025Article
- CHIRP-Seq: FOXP2 transcriptional targets in zebra finch brain include numerous speech and language-related genes.BMC neuroscience · 2025Article
- Progress of targeted FOX family therapy in ovarian cancer.Frontiers in pharmacology · 2025Review
- FOXP2 overexpression upregulates LAMA4 expression and thereby alleviates preeclampsia by regulating trophoblast behavior.Communications biology · 2024Article
- Compensation between FOXP transcription factors maintains proper striatal function.Cell reports · 2024Article
- Epigenetic control and manipulation of neuronal maturation timing.Current opinion in genetics & development · 2024Review
- Giftedness and atypical sexual differentiation: enhanced perceptual functioning through estrogen deficiency instead of androgen excess.Frontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Forkhead box P2 (FOXP2) is a transcription factor expressed in the human brain that peaks during fetal development, and disruption in its ability to regulate downstream target genes leads to vulnerability to neurodevelopmental disorders. However, the mechanisms by which FOXP2 exerts regulatory control over targets during neuronal maturation have not been fully elucidated. Here, we use genome-wide chromatin accessibility assays and transcriptome-wide expression analyses in differentiating human neurons to show that FOXP2 represses proliferation-promoting genes in a DNA-binding-dependent manner. In contrast, FOXP2 and its cofactors, NFIA and NFIB, activate neuronal maturation genes in a manner that does not require FOXP2 to interact with DNA directly. Moreover, comparisons with expression data from the developing human brain suggest that FOXP2 and NFIA- or NFIB-dependent chromatin alterations drive maturation of excitatory cortical neurons. Thus, FOXP2 and its NFI cofactors may be specifically important for the development of cortical circuits underlying neurodevelopmental disorders.
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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.