ArticleProceedings of the National Academy of Sciences of the United States of America2002
Physical and functional interactions of histone deacetylase 3 with TFII-I family proteins and PIASxbeta.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 94 citations in OpenAlex.
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Modeling Williams syndrome from a neurodevelopmental perspective: recent advances, model-based translational insights and future directions.World journal of pediatrics : WJP · 2026Review
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- Neuronal Gtf2i deletion alters mitochondrial and autophagic properties.Communications biology · 2023Article
- DNA methylation profiles in individuals with rare, atypical 7q11.23 CNVs correlate with GTF2I and GTF2IRD1 copy number.NPJ genomic medicine · 2023Article
- Syringic acid demonstrates an anti-inflammatory effect via modulation of the NF-κB-iNOS-COX-2 and JAK-STAT signaling pathways in methyl cellosolve-induced hepato-testicular inflammation in rats.Biochemistry and biophysics reports · 2023Article
- Review
- In individuals with Williams syndrome, dysregulation of methylation in non-coding regions of neuronal and oligodendrocyte DNA is associated with pathology and cortical development.Molecular psychiatry · 2023Article
- The complementary roles of STAT3 and STAT1 in cancer biology: insights into tumor pathogenesis and therapeutic strategies.Frontiers in immunology · 2023Review
- PIAS Factors from Rainbow Trout Control NF-κB- and STAT-Dependent Gene Expression.International journal of molecular sciences · 2021Article
- The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021Review
- Williams syndrome.Nature reviews. Disease primers · 2021Review
- TFII-I-mediated polymerase pausing antagonizes GLI2 induction by TGFβ.Nucleic acids research · 2020Article
- Article
- RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance.Cancer cell international · 2019Article
- Functional interrelationship between TFII-I and E2F transcription factors at specific cell cycle gene loci.Journal of cellular biochemistry · 2018Article
- Identification of additional loci associated with antibody response to Mycobacterium avium ssp. Paratuberculosis in cattle by GSEA-SNP analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
- The role of JAK-STAT signaling pathway and its regulators in the fate of T helper cells.Cell communication and signaling : CCS · 2017Review
- RNA-Seq analysis of Gtf2ird1 knockout epidermal tissue provides potential insights into molecular mechanisms underpinning Williams-Beuren syndrome.BMC genomics · 2016Article
- Aldose Reductase Acts as a Selective Derepressor of PPARγ and the Retinoic Acid Receptor.Cell reports · 2016Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
TFII-I family proteins are characterized structurally by the presence of multiple reiterated I-repeats, each containing a putative helix-loop-helix domain. Functionally, they behave as multifunctional transcription factors that are activated by a variety of extracellular signals. In studying their subcellular localization, we noticed that these transcription factors frequently reside in subnuclear domains/dots. Because nuclear dots are believed often to harbor components of histone deacetylase enzymes (HDACs), we investigated whether TFII-I family proteins colocalize and interact with HDACs. Here, we show that TFII-I and its related member hMusTRD1/BEN physically and functionally interact with HDAC3. The TFII-I family proteins and HDAC3 also show nearly identical expression patterns in early mouse development. Consistent with our earlier observation that TFII-I family proteins also interact with PIASxbeta, a member of the E3 ligase family involved in the small ubiquitin-like modifier (SUMO) pathway, we show further that PIASxbeta physically and functionally interacts with HDAC3 and relieves the transcriptional repression exerted by HDAC3 upon TFII-I-mediated gene activation. These results suggest a complex interplay between two posttranslational pathways-histone modification and SUMOylation-brokered in part by TFII-I family proteins.
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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.