ArticleCell reports2024
Compensation between FOXP transcription factors maintains proper striatal function.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Beyond the canonical view: steroid receptor network plasticity and mechanosensitive chromatin integration in breast cancer.NAR cancer · 2026Review
- Molecular and cell type-specific determinants of inferior colliculus development and auditory function.bioRxiv : the preprint server for biology · 2026Article
- Fine mapping of PTSD GWAS reveals a role for amygdalabioRxiv : the preprint server for biology · 2026Article
- FOXP1 is differentially active during development of murine vasopressin and oxytocin magnocellular neurons.iScience · 2026Article
- AnnQ: reference-based quantification of cellular abnormality at single-cell resolution.Briefings in bioinformatics · 2026Article
- Article
- Genomic Investigations of Spoken and Written Language Abilities: A Guide to Advances in Approaches, Technologies, and Discovery.Journal of speech, language, and hearing research : JSLHR · 2025Review
- Article
- Multiplexed CRISPRi Reveals a Transcriptional Switch Between KLF Activators and Repressors in the Maturing Neocortex.bioRxiv : the preprint server for biology · 2025Article
- Spatial dynamics of mammalian brain development and neuroinflammation by multimodal tri-omics mapping.bioRxiv : the preprint server for biology · 2024Article
- The dopamine hypothesis for ADHD: An evaluation of evidence accumulated from human studies and animal models.Frontiers in psychiatry · 2024Review
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8 authors.
Funding
Abstract
Spiny projection neurons (SPNs) of the striatum are critical in integrating neurochemical information to coordinate motor and reward-based behavior. Mutations in the regulatory transcription factors expressed in SPNs can result in neurodevelopmental disorders (NDDs). Paralogous transcription factors Foxp1 and Foxp2, which are both expressed in the dopamine receptor 1 (D1) expressing SPNs, are known to have variants implicated in NDDs. Utilizing mice with a D1-SPN-specific loss of Foxp1, Foxp2, or both and a combination of behavior, electrophysiology, and cell-type-specific genomic analysis, loss of both genes results in impaired motor and social behavior as well as increased firing of the D1-SPNs. Differential gene expression analysis implicates genes involved in autism risk, electrophysiological properties, and neuronal development and function. Viral-mediated re-expression of Foxp1 into the double knockouts is sufficient to restore electrophysiological and behavioral deficits. These data indicate complementary roles between Foxp1 and Foxp2 in the D1-SPNs.
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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.