Evidence map›Paper›PMID 16766652›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Extracellular signal-regulated kinase (ERK) 5 is necessary and sufficient to specify cortical neuronal fate.

Lidong Liu, Paige Cundiff, Glen Abel, Yupeng Wang, Roland Faigle, Hiroyuki Sakagami, Mei Xu, Zhengui Xia

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  5. ERK5 Phosphorylates KInternational journal of molecular sciences · 2018
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  11. Genetic activation of ERK5 MAP kinase enhances adult neurogenesis and extends hippocampus-dependent long-term memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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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

8 authors at 1 institution in 1 country.

Lidong LiuToxicology Program, Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195, USA.
Paige Cundiff
Glen Abel
Yupeng Wang
Roland Faigle
Hiroyuki Sakagami
Mei Xu
Zhengui Xia
University of Washington · US

Funding

Restoring FMRP Phenotypes Frpm Temporal Regional and Splice- Isoforms VarationsP30HD002274 · NICHD · UNIVERSITY OF WASHINGTON · PI GURALNICK, MICHAEL J · 1985 to 2013
$33.6M
CORE--VECTOR PRODUCTIONP30DK056465 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HEIMFELD, SHELLY · 1999 to 2014
$14.9M
Pharmacological Sciences SupplementT32GM007750 · NIGMS · UNIVERSITY OF WASHINGTON · PI ATKINS, WILLIAM M · 1985 to 2023
$12.6M
Regulation and Function of ERK5 in CNS neuronsR01AG019193 · NIA · UNIVERSITY OF WASHINGTON · PI XIA, ZHENGUI · 2001 to 2010
$3.0M
NIA NIH HHS AG 19193NIA NIH HHS R01 AG019193NICHD NIH HHS P30 HD002274NICHD NIH HHS P30 HD 02274NIDDK NIH HHS DK 56465NIDDK NIH HHS P30 DK056465NIGMS NIH HHS T32 GM007750NIGMS NIH HHS T32 GM 07750
6 · The paper itself

Abstract

Multipotent cortical progenitor cells differentiate into neurons and glial cells during development; however, mechanisms governing the specification of progenitors to a neuronal fate are not well understood. Although both extrinsic and intrinsic factors regulate this process, little is known about kinase signaling mechanisms that direct neuronal fate. Here, we report that extracellular signal-regulated kinase (ERK) 5 is expressed and active in proliferating cortical progenitors. Lentiviral gene delivery of a dominant negative ERK5 or dominant negative MAP kinase kinase 5 reduced the number of neurons generated from rat cortical progenitor cells in culture, whereas constitutive activation of ERK5 increased the production of neurons. Furthermore, when cortical progenitor cells were treated with ciliary neurotrophic factor, which induces precocious glial differentiation, ERK5 activation still promoted neuronal fate while suppressing glial differentiation. Our data also indicate that ERK5 does not directly regulate proliferation or apoptosis of cultured cortical progenitors. We conclude that ERK5 is necessary and sufficient to stimulate the generation of neurons from cortical progenitors. These results suggest a previously uncharacterized function for ERK5 signaling during brain development and raise the interesting possibility that extrinsic factors may instruct cortical progenitors to become neurons by activating the ERK5 pathway.

Indexed as

AnimalsCell AdhesionCell DifferentiationCell ProliferationCells, CulturedCerebellar CortexGene Expression Regulation, EnzymologicMitogen-Activated Protein Kinase 7NeurogliaNeuronsRatsRats, Sprague-DawleyStem CellsMitogen-Activated Protein Kinase 7

Identifiers

PMID16766652
PMCPMC1480469
OpenAlexW2068856879

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.