Share This Author
A functional genetic link between distinct developmental language disorders.
The FOXP2-CNTNAP2 pathway provides a mechanistic link between clinically distinct syndromes involving disrupted language, and is found to be associated with language delays in children with autism.
Identification of the transcriptional targets of FOXP2, a gene linked to speech and language, in developing human brain.
These data provide the first insight into the functional network of genes directly regulated by FOXP2 in human brain and by evolutionary comparisons, highlighting genes likely to be involved in the development of human higher-order cognitive processes.
Foxp2 Regulates Gene Networks Implicated in Neurite Outgrowth in the Developing Brain
It is indicated that Foxp2 modulates neuronal network formation, by directly and indirectly regulating mRNAs involved in the development and plasticity of neuronal connections in primary neurons and in neuronal cell models.
Towards complete and error-free genome assemblies of all vertebrate species
The Vertebrate Genomes Project is embarked on, an effort to generate high-quality, complete reference genomes for all ~70,000 extant vertebrate species and help enable a new era of discovery across the life sciences.
Identification of FOXP2 truncation as a novel cause of developmental speech and language deficits.
Investigation of the entire coding region of FOXP2, including alternatively spliced exons, in 49 probands affected with verbal dyspraxia and the discovery of the first nonsense mutation in FoxP2 opens the door for detailed investigations of neurodevelopment in people carrying different etiological variants of the gene.
Shining a light on CNTNAP2: complex functions to complex disorders
- P. Rodenas-Cuadrado, Joses W. Ho, S. Vernes
- Psychology, BiologyEuropean Journal of Human Genetics
- 1 February 2014
The role of CNTNAP2 is examined in the context of larger neurogenetic networks during development and disorder, given what is known regarding the regulation and function of this gene.
High-throughput analysis of promoter occupancy reveals direct neural targets of FOXP2, a gene mutated in speech and language disorders.
This work represents the first identification and in vivo verification of neural targets regulated by FOXP2 that suggest roles in modulating synaptic plasticity, neurodevelopment, neurotransmission, and axon guidance and represent novel entry points into in vivo pathways that may be disturbed in speech and language disorders.
Molecular networks implicated in speech-related disorders: FOXP2 regulates the SRPX2/uPAR complex.
The existence of a transcriptional regulatory network between human FOXP2 and the SRPX2/uPAR complex provides exciting insights into molecular pathways underlying speech-related disorders.
Functional genetic analysis of mutations implicated in a human speech and language disorder.
It is hypothesize that expression of alternative isoforms of FOXP2 may provide mechanisms for post-translational regulation of transcription factor function, and explore the properties of different isoforms, resulting from alternative splicing in human brain.
FOXP2 drives neuronal differentiation by interacting with retinoic acid signaling pathways
It is found that FOXP2 drives molecular changes consistent with neuronal differentiation in a human model system and regulates key processes required for normal circuit formation such as neuronal migration and neurite outgrowth.