Evidence map›Paper›PMID 23226437›Full record

ArticlePloS one2012

Systemic perturbation of the ERK signaling pathway by the proteasome inhibitor, MG132.

Murat Cirit, Kyle G Grant, Jason M Haugh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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.

Murat CiritDepartment of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, NC, USA.
Kyle G Grant
Jason M Haugh
North Carolina State University · US

Funding

Dynamic Regulation of Growth Factor Signaling NetworksR01GM088987 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI HAUGH, JASON M. · 2010 to 2013
$1.1M
NIGMS NIH HHS GM088987NIGMS NIH HHS R01 GM088987
6 · The paper itself

Abstract

Inhibition of the ubiquitin-proteasome protein degradation pathway has been identified as a viable strategy for anti-tumor therapy based on its broad effects on cell proliferation. By the same token, the variety of elicited effects confounds the interpretation of cell-based experiments using proteasome inhibitors such as MG132. It has been proposed that MG132 treatment reduces growth factor-stimulated phosphorylation of extracellular signal-regulated kinases (ERKs), at least in part through upregulation of dual specificity phosphatases (DUSPs). Here, we show that the effects of MG132 treatment on ERK signaling are more widespread, leading to a reduction in activation of the upstream kinase MEK. This suggests that MG132 systemically perturbs the intracellular phosphoproteome, impacting ERK signaling by reducing phosphorylation status at multiple levels of the kinase cascade.

Indexed as

AnimalsComputer SimulationDual-Specificity PhosphatasesEmbryo, MammalianEnzyme ActivationFibroblast Growth FactorsFibroblastsHumansLeupeptinsMAP Kinase Signaling SystemMesodermMiceMitogen-Activated Protein Kinase KinasesNIH 3T3 CellsPhosphorylationPlatelet-Derived Growth Factorbenzyloxycarbonylleucyl-leucyl-leucine aldehydeDual-Specificity PhosphatasesFibroblast Growth FactorsLeupeptinsMitogen-Activated Protein Kinase KinasesPlatelet-Derived Growth FactorProteasome Inhibitors

Identifiers

PMID23226437
PMCPMC3511445
OpenAlexW2008498117

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.