Evidence map›Paper›PMID 10962555›Full record

ArticleOncogene2000

Influence of the human endogenous retrovirus-like element HERV-E.PTN on the expression of growth factor pleiotrophin: a critical role of a retroviral Sp1-binding site.

A M Schulte, C Malerczyk, R Cabal-Manzano, J J Gajarsa, H J List, A T Riegel, A Wellstein

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Human endogenous retroviruses and the nervous system.Handbook of clinical neurology · 2014
    Review
  12. Review
  13. Article
  14. Review
  15. Retroelements and the human genome: new perspectives on an old relation.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Review
  16. An endogenous retroviral long terminal repeat is the dominant promoter for human beta1,3-galactosyltransferase 5 in the colon.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  17. Article
  18. 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

7 authors at 2 institutions in 1 country.

A M SchulteDepartment of Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC 20007, USA.
C Malerczyk
R Cabal-Manzano
J J Gajarsa
H J List
A T Riegel
A Wellstein
Georgetown University Medical Center · USGeorgetown University · US

Funding

SPORE IN BREAST CANCERP50CA058185 · NCI · GEORGETOWN UNIVERSITY · PI DICKSON, ROBERT B. · 1992 to 2004
$4.0M
NCI NIH HHS CA58185
6 · The paper itself

Abstract

Germ line insertion of a human endogenous retrovirus-like element (HERV-E.PTN) into the growth factor pleiotrophin (PTN) gene generated a phylogenetically new promoter driving the expression of functional HERV-PTN fusion transcripts. Here we show by in situ hybridization, that HERV-PTN fusion transcripts are expressed in malignant trophoblasts (i.e. choriocarcinoma) and in the proliferative and in the invasive trophoblasts of gestational trophoblastic tissue. Additionally, a 1.9 kb fragment of the HERV-derived PTN promoter was analysed which has strong activity when transiently transfected into choriocarcinoma JEG-3 cells in contrast to HeLa cells. Deletion of the retrovirally-derived promoter portion abolished its activity and an enhancer (+443 to +486) was identified in this region. Electrophoretic mobility shift and supershift experiments identified a Sp1 binding site in this enhancer and site specific mutation of this site abolished its activity in choriocarcinoma cells. Sp1 overexpression in Drosophila SL2 cells showed that the enhancer activity is mediated via Sp1 binding in vivo. Furthermore, mutation of the Sp1 binding site reduced the activity of a promoter test fragment in choriocarcinoma cells by 80%. Our result shows that a retroviral Sp1 binding site in the PTN promoter is important for the expression of growth factor pleiotrophin in human choriocarcinoma cells. Oncogene (2000) 19, 3988 - 3998.

Indexed as

Enhancer Elements, GeneticGene Expression Regulation, NeoplasticBinding SitesCarrier ProteinsChoriocarcinomaCytokinesEndogenous RetrovirusesFemaleHeLa CellsHumansHydatidiform MoleMutagenesis, InsertionalOncogene Proteins, FusionPregnancyPromoter Regions, GeneticSp1 Transcription FactorCarrier ProteinsCytokinesOncogene Proteins, FusionpleiotrophinSp1 Transcription Factor

Identifiers

PMID10962555
OpenAlexW2322646418

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.