Evidence map›Paper›PMID 28450398›Full record

ArticleThe Journal of biological chemistry2017

Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP.

Deborah M Dickey, Neil M Otto, Lincoln R Potter

Open access · hybridAbstract readComparative Study
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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

3 authors at 1 institution in 2 countries.

Deborah M DickeyFrom the Department of Biochemistry, Molecular Biology, and Biophysics and.
Neil M OttoFrom the Department of Biochemistry, Molecular Biology, and Biophysics and.
Lincoln R PotterFrom the Department of Biochemistry, Molecular Biology, and Biophysics and potter@umn.edu.
Institute of Molecular Biology and Biophysics · RU

Funding

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
NIGMS NIH HHS R01 GM098309
6 · The paper itself

Abstract

Activating mutations in the receptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC-B, also known as Npr2 or NPR-B), increase cellular cGMP and cause skeletal overgrowth, but how these mutations affect GTP catalysis is poorly understood. The A488P and R655C mutations were compared with the known mutation V883M. Neither mutation affected GC-B concentrations. The A488P mutation decreased the EC

Indexed as

Models, MolecularMutationAdenosine TriphosphateAllosteric RegulationAmino Acid SubstitutionAtrial Natriuretic Factor Receptor BBone Diseases, DevelopmentalCyclic GMPEnzyme InhibitorsGuanosine TriphosphateHEK293 CellsHumansKineticsMutagenesis, Site-DirectedMutation, MissenseNatriuretic Peptide, C-Type2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphateAdenosine TriphosphateAtrial Natriuretic Factor Receptor BCyclic GMPEnzyme InhibitorsGuanosine TriphosphateNatriuretic Peptide, C-TypeReceptors, Atrial Natriuretic FactorRecombinant Proteinscell signalingcGMPc-type natriuretic peptideguanylate cyclase (guanylyl cyclase)natriuretic peptidephosphorylationprotein phosphorylationskeletal dysplasia

Identifiers

PMID28450398
PMCPMC5473225
OpenAlexW2609758306

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.