Evidence map›Paper›PMID 9671454›Full record

ArticleMolecular and cellular biology1998

TFII-I regulates Vbeta promoter activity through an initiator element.

V Cheriyath, C D Novina, A L Roy

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 59 citations in OpenAlex.

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  8. The complex of TFII-I, PARP1, and SFPQ proteins regulates the DYX1C1 gene implicated in neuronal migration and dyslexia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008
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  15. Comparison of TFII-I gene family members deleted in Williams-Beuren syndrome.Protein science : a publication of the Protein Society · 2004
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  17. Upstream stimulatory factors are mediators of Ca2+-responsive transcription in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
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  19. Repression of TFII-I-dependent transcription by nuclear exclusion.Proceedings of the National Academy of Sciences of the United States of America · 2001
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

V CheriyathDepartment of Pathology and Program in Immunology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
C D Novina
A L Roy
Tufts University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In our effort to understand the transcriptional regulation of naturally occurring TATA-less but initiator (Inr)-containing genes, we have employed the murine T-cell receptor Vbeta 5.2 promoter as a model. Here we show by transient-transfection assays that the Inr binding transcription factor TFII-I is required for efficient expression of the Vbeta promoter in vivo. Mutations in the Inr element that reduced binding of TFII-I also abolished the Vbeta promoter activity by ectopic TFII-I. We further biochemically identified a protease-resistant N-terminal DNA binding fragment of TFII-I, p70. When ectopically expressed, recombinant p70 bound to the Vbeta Inr element with a specificity similar to that of wild-type TFII-I. More importantly, p70, which lacks independent activation functions, behaved as a dominant negative mutant that inhibited Inr-specific function of wild-type TFII-I. However, the activation functions of p70 were restored when fused to the heterologous activation domain of the yeast activator protein GAL4. Taken together, these data suggest that TFII-I functions in vivo require an intact Inr element and that the Inr-specific transcriptional functions of TFII-I are solely dictated by its N-terminal DNA binding domain and do not require its own C-terminal activation domain.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticAnimalsBacteriaBinding SitesCOS CellsDNADNA-Binding ProteinsMiceReceptors, Antigen, T-Cell, alpha-betaRecombinant Fusion ProteinsThrombinTranscription FactorsTranscription, GeneticDNADNA-Binding ProteinsReceptors, Antigen, T-Cell, alpha-betaRecombinant Fusion ProteinsThrombinTranscription Factors

Identifiers

PMID9671454
PMCPMC109030
OpenAlexW2134850471

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.