Evidence map›Paper›PMID 22549790›Full record

ArticleThe Journal of biological chemistry2012

G proteins and autocrine signaling differentially regulate gonadotropin subunit expression in pituitary gonadotrope.

Soon-Gang Choi, Jingjing Jia, Robert L Pfeffer, Stuart C Sealfon

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. GnRH pulse frequency is decoded by distinct GαHormones (Athens, Greece) · 2026
    Article
  2. Article
  3. Actions and Roles of FSH in Germinative Cells.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. GnRH-A Key Regulator of FSH.Endocrinology · 2019
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Mathematical modeling of gonadotropin-releasing hormone signaling.Molecular and cellular endocrinology · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Soon-Gang ChoiCenter for Translational Systems Biology and the Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Jingjing Jia
Robert L Pfeffer
Stuart C Sealfon
Icahn School of Medicine at Mount Sinai · US

Funding

MOLECULAR MECHANISM OF AGONISM AT THE GNRH RECEPTORR01DK046943 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI STUART C. SEALFON · 1993 to 2026
$11.0M
NIDDK NIH HHS R01 DK046943NIDDK NIH HHS R01DK046943
6 · The paper itself

Abstract

Gonadotropin-releasing hormone (GnRH) acts at gonadotropes to direct the synthesis of the gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). The frequency of GnRH pulses determines the pattern of gonadotropin synthesis. Several hypotheses for how the gonadotrope decodes GnRH frequency to regulate gonadotropin subunit genes differentially have been proposed. However, key regulators and underlying mechanisms remain uncertain. We investigated the role of individual G proteins by perturbations using siRNA or bacterial toxins. In LβT2 gonadotrope cells, FSHβ gene induction depended predominantly on Gα(q/11), whereas LHβ expression depended on Gα(s). Specifically reducing Gα(s) signaling also disinhibited FSHβ expression, suggesting the presence of a Gα(s)-dependent signal that suppressed FSH biosynthesis. The presence of secreted factors influencing FSHβ expression levels was tested by studying the effects of conditioned media from Gα(s) knockdown and cholera toxin-treated cells on FSHβ expression. These studies and related Transwell culture experiments implicate Gα(s)-dependent secreted factors in regulating both FSHβ and LHβ gene expression. siRNA studies identify inhibinα as a Gα(s)-dependent GnRH-induced autocrine regulatory factor that contributes to feedback suppression of FSHβ expression. These results uncover differential regulation of the gonadotropin genes by Gα(q/11) and by Gα(s) and implicate autocrine and gonadotrope-gonadotrope paracrine regulatory loops in the differential induction of gonadotropin genes.

Indexed as

AnimalsAutocrine CommunicationCell LineFollicle Stimulating HormoneGene Expression RegulationGonadotropin-Releasing HormoneGonadotropinsGTP-Binding ProteinsLuteinizing HormoneMicePituitary GlandFollicle Stimulating HormoneGonadotropin-Releasing HormoneGonadotropinsGTP-Binding ProteinsLuteinizing Hormone

Identifiers

PMID22549790
PMCPMC3375576
OpenAlexW1984976529

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.