Evidence map›Paper›PMID 25851935›Full record

ReviewCurrent osteoporosis reports2015

GNAS Spectrum of Disorders.

Serap Turan, Murat Bastepe

Open access · greenAbstract readReview
In one paragraph

Review in Current osteoporosis reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
13.6field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 198 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Circular RNA circLAMC1 Promotes Liver Regeneration by Regulating the miR-138-5p/Gnai2 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Update on the medical management of fibrous dysplasia of the bone.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  15. Molecular and Clinicopathologic Impact of GNAS Variants Across Solid Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Serap TuranPediatric Endocrinology, Marmara University School of Medicine Hospital, Istanbul, Turkey, serap.turan@marmara.edu.tr.
Murat Bastepe
Marmara University · TRMassachusetts General Hospital · US

Funding

XLas Relative to Gsa in Bone and Mineral Ion MetabolismR01DK073911 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BASTEPE, MURAT · 2007 to 2020
$4.9M
NIDDK NIH HHS R01 DK073911
6 · The paper itself

Abstract

The GNAS complex locus encodes the alpha-subunit of the stimulatory G protein (Gsα), a ubiquitous signaling protein mediating the actions of many hormones, neurotransmitters, and paracrine/autocrine factors via generation of the second messenger cAMP. GNAS gives rise to other gene products, most of which exhibit exclusively monoallelic expression. In contrast, Gsα is expressed biallelically in most tissues; however, paternal Gsα expression is silenced in a small number of tissues through as-yet-poorly understood mechanisms that involve differential methylation within GNAS. Gsα-coding GNAS mutations that lead to diminished Gsα expression and/or function result in Albright's hereditary osteodystrophy (AHO) with or without hormone resistance, i.e., pseudohypoparathyroidism type-Ia/Ic and pseudo-pseudohypoparathyroidism, respectively. Microdeletions that alter GNAS methylation and, thereby, diminish Gsα expression in tissues in which the paternal Gsα allele is normally silenced also cause hormone resistance, which occurs typically in the absence of AHO, a disorder termed pseudohypoparathyroidism type-Ib. Mutations of GNAS that cause constitutive Gsα signaling are found in patients with McCune-Albright syndrome, fibrous dysplasia of bone, and different endocrine and non-endocrine tumors. Clinical features of these diseases depend significantly on the parental allelic origin of the GNAS mutation, reflecting the tissue-specific paternal Gsα silencing. In this article, we review the pathogenesis and the phenotypes of these human diseases.

Indexed as

Bone DiseasesChromograninsExonsFibrous Dysplasia of BoneGTP-Binding Protein alpha Subunits, GsHumansMutationPseudohypoparathyroidismChromograninsGNAS protein, humanGTP-Binding Protein alpha Subunits, Gs

Identifiers

PMID25851935
PMCPMC4417430
OpenAlexW1997346296

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.