ArticleProceedings of the National Academy of Sciences of the United States of America2001
Repression of TFII-I-dependent transcription by nuclear exclusion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 45 citations in OpenAlex.
- Large-scale transcriptome sequencing in broiler chickens to identify candidate genes for breast muscle weight and intramuscular fat content.Genetics, selection, evolution : GSE · 2021Article
- Genome of the pincer wasp Gonatopus flavifemur reveals unique venom evolution and a dual adaptation to parasitism and predation.BMC biology · 2021Article
- TFII-I-mediated polymerase pausing antagonizes GLI2 induction by TGFβ.Nucleic acids research · 2020Article
- Functional interrelationship between TFII-I and E2F transcription factors at specific cell cycle gene loci.Journal of cellular biochemistry · 2018Article
- Integrated analysis of recurrent properties of cancer genes to identify novel drivers.Genome biology · 2013Article
- Global analysis of gene expression in the developing brain of Gtf2ird1 knockout mice.PloS one · 2011Article
- Animal models of Williams syndrome.American journal of medical genetics. Part C, Seminars in medical genetics · 2010Review
- Determination and functional analysis of the consensus binding site for TFII-I family member BEN, implicated in Williams-Beuren syndrome.The Journal of biological chemistry · 2008Article
- Purification and characterisation of cell survival factor 1 (TCSF1) from Tetrahymena thermophila.Journal of cell communication and signaling · 2007Article
- Positive and negative regulation of the transforming growth factor beta/activin target gene goosecoid by the TFII-I family of transcription factors.Molecular and cellular biology · 2005Article
- Comparison of TFII-I gene family members deleted in Williams-Beuren syndrome.Protein science : a publication of the Protein Society · 2004Article
- GTF2IRD2 is located in the Williams-Beuren syndrome critical region 7q11.23 and encodes a protein with two TFII-I-like helix-loop-helix repeats.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Regulation of alternative splicing of Gtf2ird1 and its impact on slow muscle promoter activity.The Biochemical journal · 2003Article
- Physical and functional interactions of histone deacetylase 3 with TFII-I family proteins and PIASxbeta.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
TFII-I is an unusual transcription factor possessing both basal and signal-induced transcriptional functions. Here we report the characterization of a TFII-I-related factor (MusTRD1/BEN) that regulates transcriptional functions of TFII-I by controlling its nuclear residency. MusTRD1/BEN has five or six direct repeats, each containing helix--loop--helix motifs, and, thus, belongs to the TFII-I family of transcription factors. TFII-I and MusTRD1/BEN, when expressed individually, show predominant nuclear localization. However, when the two proteins are coexpressed ectopically, MusTRD1/BEN locates almost exclusively to the nucleus, whereas TFII-I is largely excluded from the nucleus, resulting in a loss of TFII-I-dependent transcriptional activation of the c-fos promoter. Mutation of a consensus nuclear localization signal in MusTRD1/BEN results in a reversal of nuclear residency of the two proteins and a concomitant gain of c-fos promoter activity. These data suggest a means of transcriptional repression by competition at the level of nuclear occupancy.
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