Evidence map›Paper›PMID 29287086›Full record

ArticlePloS one2017

Dose-Duration Reciprocity for G protein activation: Modulation of kinase to substrate ratio alters cell signaling.

Kang-Ling Liao, Charles E Melvin, Rosangela Sozzani, Roger D Jones, Timothy C Elston, Alan M Jones

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Molecular switch architecture determines response properties of signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. 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

6 authors at 3 institutions in 1 country.

Kang-Ling LiaoDepartments of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.
Charles E MelvinDepartment of Plant and Microbial Biology, North Carolina State University, Raleigh, NC, United States of America.
Rosangela SozzaniDepartment of Plant and Microbial Biology, North Carolina State University, Raleigh, NC, United States of America.
Roger D JonesCenter for Complex Systems and Enterprises, Stevens Institute of Technology, Hoboken, NJ, United States of America.
Timothy C ElstonDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.
Alan M JonesDepartments of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.ORCID 0000-0002-2365-6462
University of North Carolina at Chapel Hill · USNorth Carolina State University · USStevens Institute of Technology · US

Funding

Novel Mechanisms Regulating the Heterotrimeric G Protein ComplexR01GM065989 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JONES, ALAN M. · 2002 to 2023
$5.5M
Spatiotemporal modeling of signal transduction in yeastR01GM079271 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ELSTON, TIMOTHY C, ERREDE, BEVERLY · 2006 to 2017
$4.0M
NIGMS NIH HHS R01 GM065989NIGMS NIH HHS R01 GM079271NIH HHS R01GM065989NIH HHS R01GM079271
6 · The paper itself

Abstract

In animal cells, activation of heterotrimeric G protein signaling generally occurs when the system's cognate signal exceeds a threshold, whereas in plant cells, both the amount and the exposure time of at least one signal, D-glucose, are used toward activation. This unusual signaling property called Dose-Duration Reciprocity, first elucidated in the genetic model Arabidopsis thaliana, is achieved by a complex that is comprised of a 7-transmembrane REGULATOR OF G SIGNALING (RGS) protein (AtRGS1), a Gα subunit that binds and hydrolyzes nucleotide, a Gβγ dimer, and three WITH NO LYSINE (WNK) kinases. D-glucose is one of several signals such as salt and pathogen-derived molecular patterns that operates through this protein complex to activate G protein signaling by WNK kinase transphosphorylation of AtRGS1. Because WNK kinases compete for the same substrate, AtRGS1, we hypothesize that activation is sensitive to the AtRGS1 amount and that modulation of the AtRGS1 pool affects the response to the stimulant. Mathematical simulation revealed that the ratio of AtRGS1 to the kinase affects system sensitivity to D-glucose, and therefore illustrates how modulation of the cellular AtRGS1 level is a means to change signal-induced activation. AtRGS1 levels change under tested conditions that mimic physiological conditions therefore, we propose a previously-unknown mechanism by which plants react to changes in their environment.

Indexed as

Signal TransductionArabidopsisArabidopsis ProteinsGenotypeGTP-Binding ProteinsPhosphorylationPhosphotransferasesSubstrate SpecificityArabidopsis ProteinsGTP-Binding ProteinsPhosphotransferases

Identifiers

PMID29287086
PMCPMC5747438
OpenAlexW2778009052

What OpenQuestion 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 OpenQuestion graph.