ArticleMolecular and cellular biology2005
Inhibition of TFII-I-dependent cell cycle regulation by p53.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 35 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
- Loss of GTF2I promotes neuronal apoptosis and synaptic reduction in human cellular models of neurodevelopment.Cell reports · 2024Article
- Neuronal Gtf2i deletion alters mitochondrial and autophagic properties.Communications biology · 2023Article
- Identification of a peptide ligand for human ALDH3A1 through peptide phage display: Prediction and characterization of protein interaction sites and inhibition of ALDH3A1 enzymatic activity.Frontiers in molecular biosciences · 2023Article
- Williams syndrome.Nature reviews. Disease primers · 2021Review
- Regulation of RNA Polymerase II Transcription Initiation and Elongation by Transcription Factor TFII-I.Frontiers in molecular biosciences · 2021Review
- Functional interrelationship between TFII-I and E2F transcription factors at specific cell cycle gene loci.Journal of cellular biochemistry · 2018Article
- Pathophysiology of TFII-I: Old Guard Wearing New Hats.Trends in molecular medicine · 2017Review
- DNA damage response defect in Williams-Beuren syndrome.International journal of molecular medicine · 2017Article
- Article
- Genome-wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity.PloS one · 2015Article
- A specific missense mutation in GTF2I occurs at high frequency in thymic epithelial tumors.Nature genetics · 2014Article
- Role of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair.British journal of cancer · 2013Article
- Review
- Loss of cell surface TFII-I promotes apoptosis in prostate cancer cells stimulated with activated α₂ -macroglobulin.Journal of cellular biochemistry · 2011Article
- Expression of the transcription factor, TFII-I, during post-implantation mouse embryonic development.BMC research notes · 2010Article
- Essential role of the N-terminal region of TFII-I in viability and behavior.BMC medical genetics · 2010Article
- Williams-Beuren syndrome-associated transcription factor TFII-I regulates osteogenic marker genes.The Journal of biological chemistry · 2009Article
- Transcriptional repression of the prosurvival endoplasmic reticulum chaperone GRP78/BIP by E2F1.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The multifunctional transcription factor TFII-I is tyrosine phosphorylated in response to extracellular growth signals and transcriptionally activates growth-promoting genes. However, whether activation of TFII-I also directly affects the cell cycle profile is unknown. Here we show that under normal growth conditions, TFII-I is recruited to the cyclin D1 promoter and transcriptionally activates this gene. Most strikingly, upon cell cycle arrest resulting from genotoxic stress and p53 activation, TFII-I is ubiquitinated and targeted for proteasomal degradation in a p53- and ATM (ataxia telangiectasia mutated)-dependent manner. Consistent with a direct role of TFII-I in cell cycle regulation and cellular proliferation, stable and ectopic expression of wild-type TFII-I increases cyclin D1 levels, resulting in accelerated entry to and exit from S phase, and overcomes p53-mediated cell cycle arrest, despite radiation. We further show that the transcriptional regulation of cyclin D1 and cell cycle control by TFII-I are dependent on its tyrosine phosphorylation at positions 248 and 611, sites required for its growth signal-mediated transcriptional activity. Taken together, our data define TFII-I as a growth signal-dependent transcriptional activator that is critical for cell cycle control and proliferation and further reveal that genotoxic stress-induced degradation of TFII-I results in cell cycle arrest.
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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.