Evidence map›Paper›PMID 28073913›Full record

ArticleThe Journal of biological chemistry2017

Raf Kinases Are Essential for Phosphate Induction of ERK1/2 Phosphorylation in Hypertrophic Chondrocytes and Normal Endochondral Bone Development.

Garyfallia Papaioannou, Elizabeth T Petit, Eva S Liu, Manuela Baccarini, Catrin Pritchard, Marie B Demay

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Phosphate homeostasis and endocrine regulators.Pediatric nephrology (Berlin, Germany) · 2026
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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 5 institutions in 3 countries.

Garyfallia PapaioannouEndocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114; Harvard Medical School, Boston, Massachusetts 02115.
Elizabeth T PetitEndocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114.
Eva S LiuEndocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114; Harvard Medical School, Boston, Massachusetts 02115; Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Manuela BaccariniDepartment of Microbiology, Immunobiology and Genetics, Center of Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Doktor-Bohr-Gasse 9, Vienna 1030, Austria.
Catrin PritchardDepartment of Molecular and Cell Biology, University of Leicester, University Road, Leicester LE1 7RH, United Kingdom.
Marie B DemayEndocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114; Harvard Medical School, Boston, Massachusetts 02115. Electronic address: demay@helix.mgh.harvard.edu.
Harvard University · USBrigham and Women's Hospital · USMassachusetts General Hospital · USUniversity of Leicester · GBUniversity of Vienna · AT

Funding

TRAINING GRANT IN ACADEMIC ENDOCRINOLOGYT32DK007529 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Ursula B. Kaiser, Anand Vaidya · 1986 to 2026
$6.3M
VITAMIN D RECEPTOR ABLATION: DIRECT AND INDIRECT CONSEQUENCESR01DK046974 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI DEMAY, MARIE · 1993 to 2015
$5.0M
Skeletal Phenotyping CoreP30AR066261 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI KRONENBERG, HENRY M. · 2014 to 2018
$3.5M
Etiology and Therapy of Rickets in the Hyp mouse model of XLHR01AR061376 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DEMAY, MARIE · 2011 to 2015
$1.9M
Molecular and cellular determinants of enthesopathy in X-linked hypophosphatemiaK08AR067854 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LIU, EVA S. · 2015 to 2019
$699k
Austrian Science Fund FWF W 1261Cancer Research UK 13083NIAMS NIH HHS K08 AR067854NIAMS NIH HHS P30 AR066261NIAMS NIH HHS R01 AR061376NIDDK NIH HHS R01 DK046974NIDDK NIH HHS T32 DK007529
6 · The paper itself

Abstract

Hypophosphatemia causes rickets by impairing hypertrophic chondrocyte apoptosis. Phosphate induction of MEK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is required for phosphate-mediated apoptosis and growth plate maturation. MEK1/2 can be activated by numerous molecules including Raf isoforms. A- and B-Raf ablation in chondrocytes does not alter skeletal development, whereas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vascularization of the growth plate. However, ablation of C-Raf does not impair phosphate-induced ERK1/2 phosphorylation

Indexed as

ChondrogenesisAnimalsApoptosisBone DevelopmentCells, CulturedChondrocytesGrowth PlateMice, Inbred C57BLMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphatesPhosphorylationProtein IsoformsProto-Oncogene Proteins A-rafProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafBraf protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphatesProtein IsoformsProto-Oncogene Proteins A-rafProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafraf Kinasesapoptosiscaspasechondrocytegrowth platephosphateRaf kinaserickets

Identifiers

PMID28073913
PMCPMC5336153
OpenAlexW2570632995

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.