ArticleScientific reports2016
The language-related transcription factor FOXP2 is post-translationally modified with small ubiquitin-like modifiers.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- DNA binding and mitotic phosphorylation protect polyglutamine proteins from assembly formation.Cell · 2025Article
- Rare loss-of-function variants in HECTD2 and AKAP11 confer risk of bipolar disorder.Nature genetics · 2025Article
- The role of cerebellar FOXP1 in the development of motor and communicative behaviors in mice.Genes, brain, and behavior · 2024Article
- Review
- DNA facilitates heterodimerization between human transcription factors FoxP1 and FoxP2 by increasing their conformational flexibility.iScience · 2023Article
- The Genetic and Molecular Basis of Developmental Language Disorder: A Review.Children (Basel, Switzerland) · 2022Review
- Molecular networks of the FOXP2 transcription factor in the brain.EMBO reports · 2021Review
- Whole-genome sequencing identifies functional noncoding variation in SEMA3C that cosegregates with dyslexia in a multigenerational family.Human genetics · 2021Article
- Heterozygous variants that disturb the transcriptional repressor activity of FOXP4 cause a developmental disorder with speech/language delays and multiple congenital abnormalities.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- PIAS1 modulates striatal transcription, DNA damage repair, and SUMOylation with relevance to Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- GATAD2B-associated neurodevelopmental disorder (GAND): clinical and molecular insights into a NuRD-related disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2020Article
- The role of SUMOylation during development.Biochemical Society transactions · 2020Review
- Dissecting FOXP2 Oligomerization and DNA Binding.Angewandte Chemie (International ed. in English) · 2019Article
- CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language.Nature communications · 2018Article
- FOXP3 Activates SUMO-ConjugatingInternational journal of molecular sciences · 2018Article
- The untold stories of the speech gene, theGenes & cancer · 2018Review
- Foxp1 regulation of neonatal vocalizations via cortical development.Genes & development · 2017Article
- Analysis of SUMO1-conjugation at synapses.eLife · 2017Article
- SUMOylation of FOXP1 regulates transcriptional repression via CtBP1 to drive dendritic morphogenesis.Scientific reports · 2017Article
- Sumoylation in Synaptic Function and Dysfunction.Frontiers in synaptic neuroscience · 2016Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations affecting the transcription factor FOXP2 cause a rare form of severe speech and language disorder. Although it is clear that sufficient FOXP2 expression is crucial for normal brain development, little is known about how this transcription factor is regulated. To investigate post-translational mechanisms for FOXP2 regulation, we searched for protein interaction partners of FOXP2, and identified members of the PIAS family as novel FOXP2 interactors. PIAS proteins mediate post-translational modification of a range of target proteins with small ubiquitin-like modifiers (SUMOs). We found that FOXP2 can be modified with all three human SUMO proteins and that PIAS1 promotes this process. An aetiological FOXP2 mutation found in a family with speech and language disorder markedly reduced FOXP2 SUMOylation. We demonstrate that FOXP2 is SUMOylated at a single major site, which is conserved in all FOXP2 vertebrate orthologues and in the paralogues FOXP1 and FOXP4. Abolishing this site did not lead to detectable changes in FOXP2 subcellular localization, stability, dimerization or transcriptional repression in cellular assays, but the conservation of this site suggests a potential role for SUMOylation in regulating FOXP2 activity in vivo.
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