Evidence map›Paper›PMID 28523267›Full record

ArticleFrontiers in cell and developmental biology2017

A Novel Role for the BMP Antagonist Noggin in Sensitizing Cells to Non-canonical Wnt-5a/Ror2/Disheveled Pathway Activation.

Ondrej Bernatik, Tomasz Radaszkiewicz, Martin Behal, Zankruti Dave, Florian Witte, Annika Mahl, Nicole H Cernohorsky, Pavel Krejci, Sigmar Stricker, Vitezslav Bryja

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  9. Bone & joint research · 2021
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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

10 authors at 2 institutions in 2 countries.

Ondrej BernatikFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Tomasz RadaszkiewiczFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Martin BehalFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Zankruti DaveFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Florian WitteInstitute for Chemistry and Biochemistry, Freie Universität BerlinBerlin, Germany.
Annika MahlInstitute for Chemistry and Biochemistry, Freie Universität BerlinBerlin, Germany.
Nicole H CernohorskyDepartment of Biology, Faculty of Medicine, Masaryk UniversityBrno, Czechia.
Pavel KrejciFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Sigmar StrickerInstitute for Chemistry and Biochemistry, Freie Universität BerlinBerlin, Germany.
Vitezslav BryjaFaculty of Sciences, Institute of Experimental Biology, Masaryk UniversityBrno, Czechia.
Masaryk University · CZFreie Universität Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian limb development is driven by the integrative input from several signaling pathways; a failure to receive or a misinterpretation of these signals results in skeletal defects. The brachydactylies, a group of overlapping inherited human hand malformation syndromes, are mainly caused by mutations in BMP signaling pathway components. Two closely related forms, Brachydactyly type B2 (BDB2) and BDB1 are caused by mutations in the BMP antagonist Noggin (NOG) and the atypical receptor tyrosine kinase ROR2 that acts as a receptor in the non-canonical Wnt pathway. Genetic analysis of Nog and Ror2 functional interaction via crossing Noggin and Ror2 mutant mice revealed a widening of skeletal elements in compound but not in any of the single mutants, thus indicating genetic interaction. Since ROR2 is a non-canonical Wnt co-receptor specific for Wnt-5a we speculated that this phenotype might be a result of deregulated Wnt-5a signaling activation, which is known to be essential for limb skeletal elements growth and patterning. We show that Noggin potentiates activation of the Wnt-5a-Ror2-Disheveled (Dvl) pathway in mouse embryonic fibroblast (MEF) cells in a Ror2-dependent fashion. Rat chondrosarcoma chondrocytes (RCS), however, are not able to respond to Noggin in this fashion unless growth arrest is induced by FGF2. In summary, our data demonstrate genetic interaction between Noggin and Ror2 and show that Noggin can sensitize cells to Wnt-5a/Ror2-mediated non-canonical Wnt signaling, a feature that in cartilage may depend on the presence of active FGF signaling. These findings indicate an unappreciated function of Noggin that will help to understand BMP and Wnt/PCP signaling pathway interactions.

Indexed as

BMP signalingbrachydactylynogginnon-canonical Wnt pathwaysRor2Wnt5a

Identifiers

PMID28523267
PMCPMC5415574
OpenAlexW2610630798

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.