Evidence map›Paper›PMID 29471062›Full record

ArticleBone2018

Constitutive stimulatory G protein activity in limb mesenchyme impairs bone growth.

Anara Karaca, Vijayram Reddy Malladi, Yan Zhu, Olta Tafaj, Elena Paltrinieri, Joy Y Wu, Qing He, Murat Bastepe

Abstract read
In one paragraph

Article in Bone, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Imprinting and skeletal disorders: lessons from pseudohypoparathyroidism and related disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Review
  2. Frontiers in endocrinology · 2023
    Review
  3. Article
  4. 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

8 authors at 2 institutions in 1 country.

Anara KaracaEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Vijayram Reddy MalladiEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Yan ZhuEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Olta TafajEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Elena PaltrinieriEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Joy Y WuEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Division of Endocrinology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Qing HeEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Murat BastepeEndocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: bastepe@helix.mgh.harvard.edu.
Harvard University · USMassachusetts General Hospital · US

Funding

TRAINING PROGRAM IN ENDOCRINOLOGY AND DIABETEST32DK007028 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Karen K Miller · 1986 to 2026
$18.5M
XLas Relative to Gsa in Bone and Mineral Ion MetabolismR01DK073911 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BASTEPE, MURAT · 2007 to 2020
$4.9M
Skeletal Phenotyping CoreP30AR066261 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI KRONENBERG, HENRY M. · 2014 to 2018
$3.5M
Sclerostin and Gsalpha signaling in osteoblastsR03AR059942 · NIAMS · STANFORD UNIVERSITY · PI WU, JOY Y · 2010 to 2012
$235k
NIAMS NIH HHS P30 AR066261NIAMS NIH HHS R03 AR059942NIDDK NIH HHS R01 DK073911NIDDK NIH HHS T32 DK007028
6 · The paper itself

Abstract

GNAS mutations leading to constitutively active stimulatory G protein alpha-subunit (Gsα) cause different tumors, fibrous dysplasia of bone, and McCune-Albright syndrome, which are typically not associated with short stature. Enhanced signaling of the parathyroid hormone/parathyroid hormone-related peptide receptor, which couples to multiple G proteins including Gsα, leads to short bones with delayed endochondral ossification. It has remained unknown whether constitutive Gsα activity also impairs bone growth. Here we generated mice expressing a constitutively active Gsα mutant (Gsα-R201H) conditionally upon Cre recombinase (cGsα

Indexed as

AnimalsBone DevelopmentCells, CulturedChromograninsCyclic AMPFemaleGTP-Binding Protein alpha Subunits, GsIntegrasesMaleMesenchymal Stem CellsMesodermMiceMice, TransgenicOsteogenesisPseudohypoparathyroidismTamoxifenChromograninsCre recombinaseCyclic AMPGnas protein, mouseGTP-Binding Protein alpha Subunits, GsIntegrasesTamoxifencAMPGNASG proteinSkeletal developmentStimulatory G protein

Identifiers

PMID29471062
PMCPMC5878747
OpenAlexW2790953129

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.