Evidence map›Paper›PMID 28964968›Full record

ArticleCellular signalling2017

Dephosphorylation is the mechanism of fibroblast growth factor inhibition of guanylyl cyclase-B.

Jerid W Robinson, Jeremy R Egbert, Julia Davydova, Hannes Schmidt, Laurinda A Jaffe, Lincoln R Potter

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  3. Review
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  5. Guanylyl cyclase-A phosphorylation decreases cardiac hypertrophy and improves systolic function in male, but not female, mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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 3 institutions in 2 countries.

Jerid W RobinsonDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, USA.
Jeremy R EgbertDepartment of Cell Biology, University of Connecticut Health Center, Farmington, CT, USA.
Julia DavydovaDepartment of Surgery, University of Minnesota, Minneapolis, MN, USA.
Hannes SchmidtInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Laurinda A JaffeDepartment of Cell Biology, University of Connecticut Health Center, Farmington, CT, USA. Electronic address: ljaffe@uchc.edu.
Lincoln R PotterDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, USA; Department of Pharmacology, University of Minnesota, Minneapolis, MN, USA. Electronic address: potter@umn.edu.
University of Minnesota · USUConn Health · USUniversity of Tübingen · DE

Funding

Signal Transduction at FertilizationR37HD014939 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI JAFFE, LAURINDA A. · 2014 to 2023
$4.8M
TRAINING GRANT IN DIABETES, ENDOCRINOLOGY, &METABOLISMT32DK007203 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LISA Senye CHOW, Douglas G Mashek · 1986 to 2026
$4.3M
Novel Theranostics for Pancreatic CancerR01CA174861 · NCI · UNIVERSITY OF MINNESOTA · PI DAVYDOVA, JULIA · 2014 to 2018
$1.6M
Regulation of guanylyl cyclase A and B by hormones, ATP and phosphorylationR01GM098309 · NIGMS · UNIVERSITY OF MINNESOTA · PI POTTER, LINCOLN ROSS · 2013 to 2016
$1.1M
NCI NIH HHS R01 CA174861NICHD NIH HHS R37 HD014939NIDDK NIH HHS T32 DK007203NIGMS NIH HHS R01 GM098309
6 · The paper itself

Abstract

Activating mutations in fibroblast growth factor receptor 3 (FGFR3) and inactivating mutations of guanylyl cyclase-B (GC-B, also called NPRB or NPR2) cause dwarfism. FGF exposure inhibits GC-B activity in a chondrocyte cell line, but the mechanism of the inactivation is not known. Here, we report that FGF exposure causes dephosphorylation of GC-B in rat chondrosarcoma cells, which correlates with a rapid, potent and reversible inhibition of C-type natriuretic peptide-dependent activation of GC-B. Cells expressing a phosphomimetic mutant of GC-B that cannot be inactivated by dephosphorylation because it contains glutamate substitutions for all known phosphorylation sites showed no decrease in GC-B activity in response to FGF. We conclude that FGF rapidly inactivates GC-B by a reversible dephosphorylation mechanism, which may contribute to the signaling network by which activated FGFR3 causes dwarfism.

Indexed as

AnimalsAtrial Natriuretic Factor Receptor BChondrocytesCyclic GMPDisease Models, AnimalDwarfismGlutamic AcidHumansNatriuretic Peptide, C-TypePhosphorylationRatsReceptor, Fibroblast Growth Factor, Type 3Receptors, Atrial Natriuretic FactorSignal TransductionAtrial Natriuretic Factor Receptor BCyclic GMPGlutamic AcidNatriuretic Peptide, C-TypeReceptor, Fibroblast Growth Factor, Type 3Receptors, Atrial Natriuretic FactorAchondroplasiaC-type natriuretic peptideCyclic GMPDwarfismFibroblast growth factorGuanylyl cyclaseNPR2

Identifiers

PMID28964968
PMCPMC5651182
OpenAlexW2756599354

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.