ArticleProtein science : a publication of the Protein Society2004
Comparison of TFII-I gene family members deleted in Williams-Beuren syndrome.
Article in Protein science : a publication of the Protein Society, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 43 citations in OpenAlex.
- Modeling Williams syndrome from a neurodevelopmental perspective: recent advances, model-based translational insights and future directions.World journal of pediatrics : WJP · 2026Review
- Williams syndrome.Nature reviews. Disease primers · 2021Review
- Interactions between polyphenolic antioxidants quercetin and naringenin dictate the distinctive redox-related chemical and biological behaviour of their mixtures.Scientific reports · 2021Article
- Review
- Mutant GTF2I induces cell transformation and metabolic alterations in thymic epithelial cells.Cell death and differentiation · 2020Article
- Functions of Gtf2i and Gtf2ird1 in the developing brain: transcription, DNA binding and long-term behavioral consequences.Human molecular genetics · 2020Article
- Neurobiology of social behavior abnormalities in autism and Williams syndrome.Nature neuroscience · 2016Review
- A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity.PloS one · 2015Article
- Genomic and proteomic analysis of transcription factor TFII-I reveals insight into the response to cellular stress.Nucleic acids research · 2014Article
- GTF2IRD2 from the Williams-Beuren critical region encodes a mobile-element-derived fusion protein that antagonizes the action of its related family members.Journal of cell science · 2012Article
- A putative polypeptide N-acetylgalactosaminyltransferase/Williams-Beuren syndrome chromosome region 17 (WBSCR17) regulates lamellipodium formation and macropinocytosis.The Journal of biological chemistry · 2012Article
- Review
- SUMOylation of GTF2IRD1 regulates protein partner interactions and ubiquitin-mediated degradation.PloS one · 2012Article
- Expression of the transcription factor, TFII-I, during post-implantation mouse embryonic development.BMC research notes · 2010Article
- Copy number variants at Williams-Beuren syndrome 7q11.23 region.Human genetics · 2010Review
- Williams-Beuren syndrome-associated transcription factor TFII-I regulates osteogenic marker genes.The Journal of biological chemistry · 2009Article
- Essential functions of the Williams-Beuren syndrome-associated TFII-I genes in embryonic development.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Identification of the TFII-I family target genes in the vertebrate genome.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Reduced fear and aggression and altered serotonin metabolism in Gtf2ird1-targeted mice.Genes, brain, and behavior · 2008Article
- Severe expressive-language delay related to duplication of the Williams-Beuren locus.The New England journal of medicine · 2005Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Williams-Beuren syndrome (WBS) is a neurological disorder resulting from a microdeletion, typically 1.5 megabases in size, at 7q11.23. Atypical patients implicate genes at the telomeric end of this multigene deletion as the main candidates for the pathology of WBS in particular the unequal cognitive profile associated with the condition. We recently identified a gene (GTF2IRD2) that shares homology with other members of a unique family of transcription factors (TFII-I family), which reside in the critical telomeric region. Using bioinformatics tools this study focuses on the detailed assessment of this gene family, concentrating on their characteristic structural components such as the leucine zipper (LZ) and I-repeat elements, in an attempt to identify features that could aid functional predictions. Phylogenetic analysis identified distinct I-repeat clades shared between family members. Linking functional data to one such clade has implicated them in DNA binding. The identification of PEST, synergy control motifs, and sumoylation sites common to all family members suggest a shared mechanism regulating the stability and transcriptional activity of these factors. In addition, the identification/isolation of short truncated isoforms for each TFII-I family member implies a mode of self-regulation. The exceptionally high identity shared between GTF2I and GTF2IRD2, suggests that heterodimers as well as homodimers are possible, and indicates overlapping functions between their respective short isoforms. Such cross-reactivity between GTF2I and GTF2IRD2 short isoforms might have been the evolutionary driving force for the 7q11.23 chromosomal rearrangement not present in the syntenic region in mice.
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