Evidence map›Paper›PMID 20709790›Full record

ArticleEukaryotic cell2010

The ROCO kinase QkgA is necessary for proliferation inhibition by autocrine signals in Dictyostelium discoideum.

Jonathan E Phillips, Richard H Gomer

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-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

23 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  3. Two endogenousProceedings of the National Academy of Sciences of the United States of America · 2025
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  5. Starvation Induces Extracellular Accumulation of Polyphosphate inInternational journal of molecular sciences · 2023
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  6. Structured foraging of soil predators unveils functional responses to bacterial defenses.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  7. An altered transcriptome underliesFrontiers in genetics · 2022
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  9. Altered protein secretion in Batten disease.Disease models & mechanisms · 2021
    Review
  10. UsingFrontiers in cell and developmental biology · 2021
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  11. Article
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  15. Review
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  18. Dipeptidyl peptidase IV is a human and murine neutrophil chemorepellent.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  19. Article
  20. A secreted protein is an endogenous chemorepellant in Dictyostelium discoideum.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

2 authors at 2 institutions in 1 country.

Jonathan E PhillipsDepartment of Biology, Texas A&M University, College Station, 77843, USA.
Richard H Gomer
Rice University · USTexas A&M University · US

Funding

An autocrine repressor of cell proliferationR01GM074990 · NIGMS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI GOMER, RICHARD H · 2006 to 2009
$1.1M
NIGMS NIH HHS GM074990NIGMS NIH HHS R01 GM074990
6 · The paper itself

Abstract

AprA and CfaD are secreted proteins that function as autocrine signals to inhibit cell proliferation in Dictyostelium discoideum. Cells lacking AprA or CfaD proliferate rapidly, and adding AprA or CfaD to cells slows proliferation. Cells lacking the ROCO kinase QkgA proliferate rapidly, with a doubling time 83% of that of the wild type, and overexpression of a QkgA-green fluorescent protein (GFP) fusion protein slows cell proliferation. We found that qkgA(-) cells accumulate normal levels of extracellular AprA and CfaD. Exogenous AprA or CfaD does not slow the proliferation of cells lacking qkgA, and expression of QkgA-GFP in qkgA(-) cells rescues this insensitivity. Like cells lacking AprA or CfaD, cells lacking QkgA tend to be multinucleate, accumulate nuclei rapidly, and show a mass and protein accumulation per nucleus like those of the wild type, suggesting that QkgA negatively regulates proliferation but not growth. Despite their rapid proliferation, cells lacking AprA, CfaD, or QkgA expand as a colony on bacteria less rapidly than the wild type. Unlike AprA and CfaD, QkgA does not affect spore viability following multicellular development. Together, these results indicate that QkgA is necessary for proliferation inhibition by AprA and CfaD, that QkgA mediates some but not all of the effects of AprA and CfaD, and that QkgA may function downstream of these proteins in a signal transduction pathway regulating proliferation.

Indexed as

Autocrine CommunicationAnimalsCell ProliferationDictyosteliumGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsMicroscopy, FluorescenceMicroscopy, VideoProtein KinasesProtozoan ProteinsRecombinant ProteinsSignal TransductionGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsProtein KinasesProtozoan ProteinsRecombinant Proteins

Identifiers

PMID20709790
PMCPMC2950431
OpenAlexW2135306929

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.