Evidence map›Paper›PMID 17519015›Full record

ArticleBMC molecular biology2007

Important roles of multiple Sp1 binding sites and epigenetic modifications in the regulation of the methionine sulfoxide reductase B1 (MsrB1) promoter.

Antonella De Luca, Paolo Sacchetta, Marzia Nieddu, Carmine Di Ilio, Bartolo Favaloro

Open access · hybridAbstract readComparative Study
In one paragraph

Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Selenoproteins in colon cancer.Free radical biology & medicine · 2018
    Review
  5. Article
  6. Selenite and ebselen supplementation attenuates D-galactose-induced oxidative stress and increases expression of SELR and SEP15 in rat lens.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2016
    Article
  7. Article
  8. Review
  9. Article
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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

5 authors at 1 institution in 1 country.

Antonella De LucaDepartment of Biomedical Sciences, University of Chieti G, D'Annunzio School of Medicine, and Unit of Gene Regulation, Center of Excellence on Aging, G, D'Annunzio University Foundation, Chieti, Italy. atdeluca@unich.it <atdeluca@unich.it>
Paolo Sacchetta
Marzia Nieddu
Carmine Di Ilio
Bartolo Favaloro
University of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMethionine sulfoxide reductases (Msrs) are enzymes that catalyze the reduction of oxidized methionine residues. Most organisms that were genetically modified to lack the MsrA gene have shown shortening of their life span. Methionine sulfoxide reductases B (MsrB) proteins codified by three separate genes, named MsrB1, MsrB2, and MsrB3, are included in the Msrs system. To date, the mechanisms responsible for the transcriptional regulation of MsrB genes have not been reported. The aim of this study was to investigate the regulation of MsrB1 selenoprotein levels through transcriptional regulation of the MsrB1 gene in MDA-MB231 and MCF-7 breast carcinoma cell lines.

resultsA MsrB1 gene promoter is located 169 base pairs upstream from the transcription start site. It contains three Sp1 binding sites which are sufficient for maximal promoter activity in transient transfection experiments. High levels of MsrB1 transcript, protein and promoter activity were detected in low metastatic MCF7 human breast cancer cells. On the contrary, very low levels of both MsrB1 transcript and promoter activity were detected in the highly metastatic counterpart MDA-MB231 cells.A pivotal role for Sp1 in the constitutive expression of the MsrB1 gene was demonstrated through transient expression of mutant MsrB1 promoter-reporter gene constructs and chromatin immunoprecipitation experiments. Since Sp1 is ubiquitously expressed, these sites, while necessary, are not sufficient to explain the patterns of gene expression of MsrB1 in various human breast cancer cells. MDA-MB231 cells can be induced to express MsrB1 by treatment with 5-Aza-2'-deoxycytidine, a demethylating agent. Therefore, the MsrB1 promoter is controlled by epigenetic modifications.

conclusionThe results of this study provide the first insights into the transcriptional regulation of the human MsrB1 gene, including the discovery that the Sp1 transcription factor may play a central role in its expression. We also demonstrated that the MsrB1 promoter activity appears to be controlled by epigenetic modifications such as methylation.

Indexed as

Binding SitesBlotting, WesternCell Line, TumorChromatin ImmunoprecipitationDNA MethylationEpigenesis, GeneticGene Expression Regulation, EnzymologicHumansMethionine Sulfoxide ReductasesMicrofilament ProteinsMutagenesis, Site-DirectedOxidoreductasesPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionSp1 Transcription FactorTranscription FactorsMethionine Sulfoxide ReductasesMicrofilament ProteinsMSRB2 protein, humanOxidoreductasesSp1 Transcription FactorTranscription Factors

Identifiers

PMID17519015
PMCPMC1885803
OpenAlexW2092478331

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.