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Forkhead box P2

FOXP2, forkhead/winged helix transcription factor
This gene encodes a member of the forkhead/winged-helix (FOX) family of transcription factors. It is expressed in fetal and adult brain as well as in several other organs such as the lung and gut. The protein product contains a FOX DNA-binding domain and a large polyglutamine tract and is an evolutionarily conserved transcription factor, which may bind directly to approximately 300 to 400 gene promoters in the human genome to regulate the expression of a variety of genes. This gene is required for proper development of speech and language regions of the brain during embryogenesis, and may be involved in a variety of biological pathways and cascades that may ultimately influence language development. Mutations in this gene cause speech-language disorder 1 (SPCH1), also known as autosomal dominant speech and language disorder with orofacial dyspraxia. Multiple alternative transcripts encoding different isoforms have been identified in this gene.[provided by RefSeq, Feb 2010] (from NCBI)
Top mentioned proteins: Foxp3, CAN, FOXP1, CD4, ACID
Papers on FOXP2
Human-specific increase of dopaminergic innervation in a striatal region associated with speech and language: A comparative analysis of the primate basal ganglia.
Sherwood et al., New York City, United States. In J Comp Neurol, Jan 2016
Several lines of evidence suggest that evolutionary changes in dopaminergic afferents of the striatum may be associated with uniquely human cognitive and behavioral abilities, including the association of the human-specific sequence of the FOXP2 gene with decreased dopamine in the dorsomedial striatum of mice.
Identification and functional characterization of de novo FOXP1 variants provides novel insights into the etiology of neurodevelopmental disorder.
Fisher et al., Nijmegen, Netherlands. In Hum Mol Genet, Jan 2016
These variants also retained the ability to interact with FOXP2, a paralogous transcription factor disrupted in rare cases of speech and language disorder.
Understanding Language from a Genomic Perspective.
Fisher et al., Nijmegen, Netherlands. In Annu Rev Genet, Dec 2015
Heritable disorders offer a gateway into biological underpinnings, as illustrated by the discovery that FOXP2 disruptions cause a rare form of speech and language impairment.
Ultrasonic vocalizations of adult male Foxp2-mutant mice: behavioral contexts of arousal and emotion.
Ehret et al., Ulm, Germany. In Genes Brain Behav, Dec 2015
Furthermore, we analyzed two mouse lines with heterozygous Foxp2 mutations (R552H missense, S321X nonsense), known to produce severe speech and language disorders in humans.
Insights into the genetic foundations of human communication.
Fisher et al., Nijmegen, Netherlands. In Neuropsychol Rev, Mar 2015
The first gene directly implicated in a speech and language disorder was FOXP2.
MSC-regulated microRNAs converge on the transcription factor FOXP2 and promote breast cancer metastasis.
Karnoub et al., Boston, United States. In Cell Stem Cell, 2015
We demonstrate that such MSC-deregulated microRNAs constitute a network that converges on and represses the expression of FOXP2, a forkhead transcription factor tightly associated with speech and language development.
Risperidone and NAP protect cognition and normalize gene expression in a schizophrenia mouse model.
Gozes et al., Tel Aviv-Yafo, Israel. In Sci Rep, 2014
Transcripts of Forkhead-BOX P2 (Foxp2), a gene regulating DISC1 and associated with human ability to acquire a spoken language, were increased in the hippocampus of the DISC1 mutated mice and were significantly lowered after treatment with NAP, Risperidone, or the combination of both.
Neanderthals did speak, but FOXP2 doesn't prove it.
Johansson, Falun, Sweden. In Behav Brain Sci, 2014
The case of FOXP2 and Neanderthals is a prime example, which I will comment on in some detail; the issues are much more complex than they appear in Ackermann et al.
Why we can talk, debate, and change our minds: neural circuits, basal ganglia operations, and transcriptional factors.
Lieberman, Providence, United States. In Behav Brain Sci, 2014
Basal ganglia operations, enhanced by mutations on FOXP2, confer human motor-control, linguistic, and cognitive capabilities.
Brain mechanisms of acoustic communication in humans and nonhuman primates: an evolutionary perspective.
Ziegler et al., München, Germany. In Behav Brain Sci, 2014
Furthermore, neurobiological and paleoanthropological data point at a two-stage model of the phylogenetic evolution of this crucial prerequisite of spoken language: (i) monosynaptic refinement of the projections of motor cortex to the brainstem nuclei that steer laryngeal muscles, presumably, as part of a "phylogenetic trend" associated with increasing brain size during hominin evolution; (ii) subsequent vocal-laryngeal elaboration of cortico-basal ganglia circuitries, driven by human-specific FOXP2 mutations.;>This
Retinoic Acid Signaling: A New Piece in the Spoken Language Puzzle.
Vernes et al., Nijmegen, Netherlands. In Front Psychol, 2014
FOXP2 was the first single gene identified to cause speech and language disorder.
Tuftsin-derived T-peptide prevents cellular immunosuppression and improves survival rate in septic mice.
Yao et al., Tianjin, China. In Sci Rep, 2014
When CD4(+)CD25(+) Tregs were treated with T-peptide for 24 hours, and co-cultured with normal CD4(+)CD25(-) T cells, the suppressive ability of CD4(+)CD25(+) Tregs on CD4(+)CD25(-) T cells was significantly lowered, along with decreased expression in forkhead/winged helix transcription factor p-3 (Foxp-3) as well as cytotoxic T lymphocyte-associated antigen (CTLA)-4, and secretion of transforming growth factor (TGF)-β.
Environments organize the verbal brain.
Catania, Baltimore, United States. In Behav Brain Sci, 2014
FOXP2 expression in the evolution of language derives from its role in allowing vocal articulation that is sensitive to its consequences.
What can mice tell us about Foxp2 function?
Fisher et al., Lisbon, Portugal. In Curr Opin Neurobiol, 2014
Disruptions of the FOXP2 gene cause a rare speech and language disorder, a discovery that has opened up novel avenues for investigating the relevant neural pathways.
Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms.
Guo, Temple, United States. In J Endocrinol, 2014
Emphasis is placed on the role of IRS1, IRS2, and associated signaling pathways that are coupled to Akt and the forkhead/winged helix transcription factor Foxo1.
Convergent repression of Foxp2 3'UTR by miR-9 and miR-132 in embryonic mouse neocortex: implications for radial migration of neurons.
De Pietri Tonelli et al., Genova, Italy. In Development, 2012
Results uncover a new layer of control of Foxp2 expression that may be required for proper neuronal maturation.
An association study of sequence variants in the forkhead box P2 (FOXP2) gene and adulthood attention-deficit/hyperactivity disorder in two European samples.
Bayés et al., Barcelona, Spain. In Psychiatr Genet, 2012
The single-marker and multiple-marker analyses showed an association between FOXP2 and combined Attention-deficit/hyperactivity disorder in the German cohort.
Genetic variants of FOXP2 and KIAA0319/TTRAP/THEM2 locus are associated with altered brain activation in distinct language-related regions.
Dehaene et al., Gif-sur-Yvette, France. In J Neurosci, 2012
The results of this study confirmed that both FOXP2 and KIAA0319/TTRAP/THEM2 genes play an important role in human language development, but probably through different cerebral pathways.
Cadm1-expressing synapses on Purkinje cell dendrites are involved in mouse ultrasonic vocalization activity.
Momoi et al., Tochigi, Japan. In Plos One, 2011
Results suggest that although the Foxp2 transcription factor does not target Cadm1, Cadm1 at the synapses of Purkinje cells and parallel fibers is necessary for ultrasonic vocalization (USV) function.
Foxp2 mutations impair auditory-motor association learning.
Ehret et al., Ulm, Germany. In Plos One, 2011
our study of etiological Foxp2 mutations in mice has revealed novel cognitive deficits that go beyond motor functions and extend to auditory-motor association learning.
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