Evidence map›Paper›PMID 21238538›Full record

ArticleMolecular and cellular endocrinology2011

Progesterone induces expression of the prolactin receptor gene through cooperative action of Sp1 and C/EBP.

Anita S Goldhar, Renqin Duan, Erika Ginsburg, Barbara K Vonderhaar

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Anita S GoldharMammary Biology and Tumorigenesis Laboratory, Center for Cancer Research, NCI, Bethesda, MD 20892-4254, USA.
Renqin Duan
Erika Ginsburg
Barbara K Vonderhaar
Center for Cancer Research · US

Funding

Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Prolactin (Prl) and progesterone (P) cooperate synergistically during mammary gland development and tumorigenesis. We hypothesized that one mechanism for these effects may be through mutual induction of receptors (R). EpH4 mouse mammary epithelial cells stably transfected with PR-A express elevated levels of PrlR mRNA and protein compared to control EpH4 cells that lack the PR. Likewise, T47D human breast cancer cells treated with P overexpress the PrlR and activate PrlR promoter III. PrlR promoter III does not contain a classical P response element but contains several binding sites for transcription proteins, including C/EBP, Sp1 and AP1, which may also interact with the PR. Using promoter deletion and site directed mutagenesis analyses as well as gel shift assays, cooperative activation of the C/EBP and adjacent Sp1A, but not the Sp1B or AP1, sites by P is shown to confer P responsiveness leading to increased PrlR transcription.

Indexed as

AnimalsCCAAT-Enhancer-Binding ProteinsCell LineCell Line, TumorGenes, ReporterHumansImmunoprecipitationLuciferasesMiceProgesteroneProtein BindingProtein IsoformsReceptors, ProgesteroneReceptors, ProlactinRecombinant ProteinsResponse ElementsCCAAT-Enhancer-Binding ProteinsLuciferasesProgesteroneProtein IsoformsReceptors, ProgesteroneReceptors, ProlactinRecombinant ProteinsSp1 Transcription Factor

Identifiers

PMID21238538
PMCPMC3045478
OpenAlexW2004966659

What OpenQuestion holds

Textmetadata
LicenceTDM
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.