Evidence map›Paper›PMID 15713647›Full record

ArticleMolecular and cellular biology2005

Loss of Gq/11 family G proteins in the nervous system causes pituitary somatotroph hypoplasia and dwarfism in mice.

N Wettschureck, A Moers, B Wallenwein, A F Parlow, C Maser-Gluth, S Offermanns

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Ghrelin Modulates Voltage-Gated CaMolecular pharmacology · 2024
    Article
  3. Review
  4. Photoperiod Induces the Epigenetic Change of theInternational journal of molecular sciences · 2023
    Article
  5. Article
  6. Article
  7. Ghrelin receptor signaling in health and disease: a biased view.Trends in endocrinology and metabolism: TEM · 2023
    Review
  8. Discovery of a functionally selective ghrelin receptor (GHSRProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Loss of Gαq impairs regulatory B-cell function.Arthritis research & therapy · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Ghrelin receptors in non-Mammalian vertebrates.Frontiers in endocrinology · 2013
    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

6 authors at 2 institutions in 2 countries.

N WettschureckInstitute of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany. Nina.Wettschureck@urz.uni-heidelberg.de
A Moers
B Wallenwein
A F Parlow
C Maser-Gluth
S Offermanns
Heidelberg University · DEUCLA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterotrimeric G proteins of the Gq/11 family transduce signals from a variety of neurotransmitter and hormone receptors and have therefore been implicated in various functions of the nervous system. Using the Cre/loxP system, we generated mice which lack the genes coding for the alpha subunits of the two main members of the Gq/11 family, gnaq and gna11, selectively in neuronal and glial precursor cells. Mice with defective gnaq and gna11 genes were morphologically normal, but they died shortly after birth. Mice carrying a single gna11 allele survived the early postnatal period but died within 3 to 6 weeks as anorectic dwarfs. In these mice, postnatal proliferation of pituitary somatotroph cells was strongly impaired, and plasma growth hormone (GH) levels were reduced to 15%. Hypothalamic levels of GH-releasing hormone (GHRH), an important stimulator of somatotroph proliferation, were strongly decreased, and exogenous administration of GHRH restored normal proliferation. The hypothalamic effects of ghrelin, a regulator of GHRH production and food intake, were reduced in these mice, suggesting that an impairment of ghrelin receptor signaling might contribute to GHRH deficiency and abnormal eating behavior. Taken together, our findings show that Gq/11 signaling is required for normal hypothalamic function and that impairment of this signaling pathway causes somatotroph hypoplasia, dwarfism, and anorexia.

Indexed as

AllelesAnimalsCell ProliferationDwarfism, PituitaryEatingGhrelinGrowth HormoneGrowth Hormone-Releasing HormoneGTP-Binding Protein alpha Subunits, Gq-G11HypothalamusMiceMice, KnockoutMutationOrgan SizePeptide HormonesPituitary GlandGhrelinGrowth HormoneGrowth Hormone-Releasing HormoneGTP-Binding Protein alpha Subunits, Gq-G11Peptide HormonesProto-Oncogene Proteins c-fos

Identifiers

PMID15713647
PMCPMC549379
OpenAlexW2151669146

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.