Evidence map›Paper›PMID 22230296›Full record

ArticleSteroids2012

Estrogen- and xenoestrogen-induced ERK signaling in pituitary tumor cells involves estrogen receptor-α interactions with G protein-αi and caveolin I.

Cheryl S Watson, Yow-Jiun Jeng, Guangzhen Hu, Ann Wozniak, Nataliya Bulayeva, Jutatip Guptarak

Abstract read
In one paragraph

Article in Steroids, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Mechanisms underlying sex differences in autoimmunity.The Journal of clinical investigation · 2024
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  6. Long-Term Follow-Up and Treatment of a Female With Complete Estrogen Insensitivity.The Journal of clinical endocrinology and metabolism · 2020
    Article
  7. Observational
  8. Article
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  10. Non-genomic Effects of Glucocorticoids: An Updated View.Trends in pharmacological sciences · 2019
    Review
  11. Crosstalk between nuclear and G protein-coupled estrogen receptors.General and comparative endocrinology · 2018
    Review
  12. Black tea andAmerican journal of translational research · 2018
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Cheryl S WatsonDept. of Biochemistry & Molecular Biology, Univ. of Texas Medical Branch, Galveston, TX 77555-0645, USA. cswatson@utmb.edu
Yow-Jiun Jeng
Guangzhen Hu
Ann Wozniak
Nataliya Bulayeva
Jutatip Guptarak
The University of Texas Medical Branch at Galveston · US

Funding

Nongenomic Signaling Mechanisms of Environmental EstrogensR01ES015292 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WATSON, CHERYL S · 2007 to 2011
$1.2M
NIEHS NIH HHS R01 ES015292
6 · The paper itself

Abstract

unlabelledMultiple physiologic estrogens (estradiol, estriol, and estrone), as well as xenoestrogenic compounds (including alkylphenols and bisphenol A), can act via nongenomic signaling initiated by liganding of the plasma membrane estrogen receptor-α (mERα). We examined heterotrimeric G protein involvement leading to extracellular-regulated kinase (ERK) activation in GH3/B6/F10 rat anterior pituitary tumor cells that express abundant mERα, and smaller amounts of mERβ and GPR30. A combination of microarrays, immunoblots, and quantitative immunoassays demonstrated the expression of members of all α, β, and γ G protein classes in these cells. Use of selective inhibitors showed that the G(αi) subtype was the primary initiator of downstream ERK signaling. Using antibodies against the GTP-bound form of G(α) protein subtypes i and s, we showed that xenoestrogens (bisphenol A, nonylphenol) activated G(αi) at 15-30s; all alkylphenols examined subsequently suppressed activation by 5min. GTP-activation of G(αi) for all estrogens was enhanced by irreversible cumulative binding to GTPγS. In contrast, G(αs) was neither activated nor deactivated by these treatments with estrogens. ERα and G(αi) co-localized outside nuclei and could be immuno-captured together. Interactions of ERα with G(αi) and caveolin I were demonstrated by epitope proximity ligation assays. An ERα/β antagonist (ICI182780) and a selective disruptor of caveolar structures (nystatin) blocked estrogen-induced ERK activation.

conclusionsXenoestrogens, like physiologic estrogens, can evoke downstream kinase signaling involving selective interactions of ERα with G(αi) and caveolin I, but with some different characteristics, which could explain their disruptive actions.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsCaveolaeCaveolin 1Cell Line, TumorCell MembraneEstrogen Receptor alphaEstrogensEstrogens, Non-SteroidalExtracellular Signal-Regulated MAP KinasesGTP-Binding Protein alpha Subunits, Gi-GoGuanosine TriphosphateImmunoblottingMAP Kinase Signaling SystemMicroscopy, FluorescenceBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCaveolin 1Estrogen Receptor alphaEstrogensEstrogens, Non-SteroidalExtracellular Signal-Regulated MAP KinasesGTP-Binding Protein alpha Subunits, Gi-GoGuanosine TriphosphatenonylphenolPhenols

Identifiers

PMID22230296
PMCPMC3304022
OpenAlexW2035345556

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.