ArticleGene2009
Alternative splicing and promoter use in TFII-I genes.
Article in Gene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Gtf2i-encoded transcription factor Tfii-i regulates myelination via Sox10 and Mbp regulatory elements.Nature communications · 2025Article
- Canine hyper-sociability structural variants associated with altered three-dimensional chromatin state.BMC genomics · 2024Article
- Deletion ofBiomedicines · 2023Article
- Pathophysiology of TFII-I: Old Guard Wearing New Hats.Trends in molecular medicine · 2017Review
- Role of Splice Variants of Gtf2i, a Transcription Factor Localizing at Postsynaptic Sites, and Its Relation to Neuropsychiatric Diseases.International journal of molecular sciences · 2017Review
- Nuclear factor-κB regulates expression of platelet phospholipase C-β2 (PLCB2).Thrombosis and haemostasis · 2016Article
- Evolution of general transcription factors.Journal of molecular evolution · 2013Article
- Association of GTF2i in the Williams-Beuren syndrome critical region with autism spectrum disorders.Journal of autism and developmental disorders · 2012Article
- Alterations of the 5'untranslated region of SLC16A12 lead to age-related cataract.Investigative ophthalmology & visual science · 2010Article
- Negative autoregulation of GTF2IRD1 in Williams-Beuren syndrome via a novel DNA binding mechanism.The Journal of biological chemistry · 2010Article
- Binding of Gtf2i-β/δ transcription factors to the ARMS2 gene leads to increased circulating HTRA1 in AMD patients and in vitro.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
TFII-I proteins are ubiquitously expressed transcriptional factors involved in both basal transcription and signal transduction activation or repression. TFII-I proteins are detected as early as at two-cell stage and exhibit distinct and dynamic expression patterns in developing embryos as well as mark regional variation in the adult mouse brain. Analysis of atypical small and rare chromosomal deletions at 7q11.23 points to TFII-I genes (GTF2I and GTF2IRD1) as the prime candidates responsible for craniofacial and cognitive abnormalities in the Williams-Beuren syndrome. TFII-I genes are often subjected to alternative splicing, which generates isoforms that show different activities and play distinct biological roles. The coding regions of TFII-I genes are composed of more than 30 exons and are well conserved among vertebrates. However, their 5' untranslated regions are not as well conserved and all poorly characterized. In the present work, we analyzed promoter regions of TFII-I genes and described their additional exons, as well as tested tissue specificity of both previously reported and novel alternatively spliced isoforms. Our comprehensive analysis leads to further elucidation of the functional heterogeneity of TFII-I proteins, provides hints on search for regulatory pathways governing their expression, and opens up possibilities for examining the effect of different haplotypes on their promoter functions.
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What OpenQuestion holds
Registered trials
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.