Evidence map›Paper›PMID 20008557›Full record

ArticleMolecular and cellular biology2010

Frequency-dependent regulation of follicle-stimulating hormone beta by pulsatile gonadotropin-releasing hormone is mediated by functional antagonism of bZIP transcription factors.

Nick A Ciccone, Shuyun Xu, Charlemagne T Lacza, Rona S Carroll, Ursula B Kaiser

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. GnRH pulse frequency is decoded by distinct GαHormones (Athens, Greece) · 2026
    Article
  2. Article
  3. Article
  4. Augmentation ofJournal of the Endocrine Society · 2020
    Article
  5. GnRH-A Key Regulator of FSH.Endocrinology · 2019
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Mathematical modeling of gonadotropin-releasing hormone signaling.Molecular and cellular endocrinology · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

5 authors at 2 institutions in 1 country.

Nick A CicconeDivision of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, 221 Longwood Ave., Boston, MA 02115, USA.
Shuyun Xu
Charlemagne T Lacza
Rona S Carroll
Ursula B Kaiser
Harvard University · USBrigham and Women's Hospital · US

Funding

The Genetic Determinants of Human GNRH DeficiencyU54HD028138 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI CROWLEY, WILLIAM FRANCIS · 2000 to 2013
$19.9M
REPRODUCTIVE PHYSIOLOGY OF LUTROPIN SYNTHESISR01HD019938 · NICHD · JOSLIN DIABETES CENTER · PI KAISER, URSULA B. · 1985 to 2017
$3.9M
Reproductive Biology of Gonadotropin RegulationR01HD033001 · NICHD · BRIGHAM AND WOMEN'S HOSPITAL · PI KAISER, URSULA B · 2001 to 2005
$1.5M
NICHD NIH HHS R01 HD019938NICHD NIH HHS R01 HD033001NICHD NIH HHS R01 HD19938NICHD NIH HHS R01 HD33001NICHD NIH HHS U54 HD028138NICHD NIH HHS U54 HD28138
6 · The paper itself

Abstract

Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. The molecular mechanisms by which various patterns of pulsatile GnRH regulate gonadotrope responsiveness remain poorly understood. In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function.

Indexed as

Adenosine MonophosphateAnimalsCell LineCyclic AMP Response Element ModulatorFollicle Stimulating Hormone, beta SubunitGene Expression RegulationGonadotropin-Releasing HormoneMicePromoter Regions, GeneticProtein BindingResponse ElementsRNA InterferenceTranscription, GeneticAdenosine MonophosphateCrem protein, mouseCyclic AMP Response Element ModulatorFollicle Stimulating Hormone, beta SubunitGonadotropin-Releasing Hormone

Identifiers

PMID20008557
PMCPMC2815570
OpenAlexW2123467533

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.