Evidence map›Paper›PMID 15479157›Full record

ArticleThe Biochemical journal2005

The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter.

Daman Kumari, Andrei Gabrielian, David Wheeler, Karen Usdin

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 38 citations in OpenAlex.

  1. Investigating Potential 5' UTR G-Quadruplexes Within NRF2 mRNA.Current issues in molecular biology · 2026
    Article
  2. Review
  3. Article
  4. DNA Methylation, Mechanisms ofBiomolecules · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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

4 authors at 2 institutions in 1 country.

Daman KumariNational Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0830, USA.
Andrei Gabrielian
David Wheeler
Karen Usdin
National Center for Biotechnology Information · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

The pathology consequences of repeat expansion in the Repeat Expansion DiseasesZIADK057602 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI USDIN, KAREN P. · 2009 to 2025
$11.5M
THE TRIPLET EXPANSION DISEASESZ01DK057602 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI USDIN, KAREN P. · 1997 to 2008
$624k
6 · The paper itself

Abstract

Expansion of a CGG.CCG-repeat tract in the 5'-untranslated region of the FMR1 (Fragile X mental retardation 1) gene causes its aberrant transcription. This produces symptoms ranging from premature ovarian failure and Fragile X associated tremor and ataxia syndrome to FMR syndrome, depending on the size of the expansion. The promoter from normal alleles shows four protein-binding regions in vivo. We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1). We also showed that these sites are involved in the positive regulation of FMR1 transcription in neuronally derived cells. In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity. We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove. The combined effect of the four protein-induced bends on promoter geometry is the formation of a highly compact arch-like structure in which the 5' end of the promoter is brought in close proximity to the 3' end. We had previously shown that while point mutations in the GC-boxes decrease promoter activity, deletion of either one of them leads to an increase in promoter activity. We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation.

Indexed as

Nucleic Acid ConformationAnimalsBase SequenceCell LineDNADNA-Binding ProteinsDogsDrosophilaFragile X Messenger Ribonucleoprotein 1HumansMacacaMiceMolecular Sequence DataNerve Tissue ProteinsNF-E2-Related Factor 1Nuclear Respiratory Factor 1DNADNA-Binding ProteinsFMR1 protein, humanFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Nerve Tissue ProteinsNF-E2-Related Factor 1NRF1 protein, humanNrf1 protein, mouseNuclear Respiratory Factor 1Nuclear Respiratory FactorsProtein IsoformsRNA-Binding ProteinsSp1 Transcription FactorSP3 protein, humanSp3 protein, mouseSp3 Transcription FactorTrans-ActivatorsTranscription FactorsUpstream Stimulatory FactorsUSF1 protein, humanUsf1 protein, mouseUSF2 protein, humanUsf2 protein, mouse

Identifiers

PMID15479157
PMCPMC1134794
OpenAlexW2006737346

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.