Evidence map›Paper›PMID 23210626›Full record

ArticleBiochemistry2013

Proper protein glycosylation promotes mitogen-activated protein kinase signal fidelity.

Evan C Lien, Michal J Nagiec, Henrik G Dohlman

Abstract read
In one paragraph

Article in Biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Putative role of TMEM165 in congenital cardiomyopathies.Frontiers in molecular neuroscience · 2025
    Review
  3. Article
  4. Article
  5. Article
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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

3 authors at 1 institution in 1 country.

Evan C LienDepartment of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Michal J Nagiec
Henrik G Dohlman
University of North Carolina at Chapel Hill · US

Funding

G Protein Signaling at the endosomeR01GM080739 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DOHLMAN, HENRIK G. · 2007 to 2014
$2.6M
NIGMS NIH HHS GM080739NIGMS NIH HHS R01 GM080739
6 · The paper itself

Abstract

The ability of cells to sense and respond appropriately to changing environmental conditions is often mediated by signal transduction pathways that employ mitogen-activated protein kinases (MAPKs). In the yeast Saccharomyces cerevisiae, the high-osmolarity glycerol (HOG) and filamentous growth (FG) pathways are activated following hyperosmotic stress and nutrient deprivation, respectively. Whereas the HOG pathway requires the MAPK Hog1, the FG pathway employs the MAPK Kss1. We conducted a comprehensive screen of nearly 5000 gene deletion strains for mutants that exhibit inappropriate cross-talk between the HOG and FG pathways. We identified two novel mutants, mnn10Δ and mnn11Δ, that allow activation of Kss1 under conditions that normally stimulate Hog1. MNN10 and MNN11 encode mannosyltransferases that are part of the N-glycosylation machinery within the Golgi apparatus; deletion of either gene results in N-glycosylated proteins that have shorter mannan chains. Deletion of the cell surface mucin Msb2 suppressed the mnn11Δ phenotype, while mutation of a single glycosylation site within Msb2 was sufficient to confer inappropriate activation of Kss1 by salt stress. These findings reveal new components of the N-glycosylation machinery needed to ensure MAPK signaling fidelity.

Indexed as

MAP Kinase Signaling SystemGene DeletionGene Expression Regulation, FungalGlycerolGlycosylationMitogen-Activated Protein KinasesOsmotic PressureSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsGlycerolMitogen-Activated Protein KinasesSaccharomyces cerevisiae Proteins

Identifiers

PMID23210626
PMCPMC3540157
OpenAlexW2076550124

What OpenQuestion holds

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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.