Evidence map›Paper›PMID 19581298›Full record

ArticleThe Journal of biological chemistry2009

ERK5 activity is required for nerve growth factor-induced neurite outgrowth and stabilization of tyrosine hydroxylase in PC12 cells.

Yutaro Obara, Arata Yamauchi, Shin Takehara, Wataru Nemoto, Maho Takahashi, Philip J S Stork, Norimichi Nakahata

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 7% 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, 70 citations in OpenAlex.

  1. Article
  2. Article
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  4. Trojan Horse Delivery of 4,4'-Dimethoxychalcone for Parkinsonian Neuroprotection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  5. Involvement of MEK5/ERK5 signaling pathway in manganese-induced cell injury in dopaminergic MN9D cells.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020
    Article
  6. Article
  7. Midnolin is a confirmed genetic risk factor for Parkinson's disease.Annals of clinical and translational neurology · 2019
    Article
  8. Article
  9. ERK5 Phosphorylates KInternational journal of molecular sciences · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. ERK5 Mediated Signalling in Diabetic Retinopathy.Medical hypothesis, discovery & innovation ophthalmology journal · 2015
    Review
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

Yutaro ObaraDepartment of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan. obaray@mail.pharm.tohoku.ac.jp
Arata Yamauchi
Shin Takehara
Wataru Nemoto
Maho Takahashi
Philip J S Stork
Norimichi Nakahata
Tohoku University · JPVollum Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular signal-regulated kinases (ERKs) play important physiological roles in proliferation, differentiation, and gene expression. ERK5 is approximately twice the size of ERK1/2, and its amino-terminal half contains the kinase domain that shares homology with ERK1/2 and TEY activation motif, whereas the carboxyl-terminal half is unique. In this study, we examined a physiological role of ERK5 in rat pheochromocytoma cells (PC12), comparing it with ERK1/2. Nerve growth factor (NGF) induced phosphorylation of both ERK5 and ERK1/2, whereas the cAMP analog dibutyryl cAMP (Bt(2)cAMP) caused only ERK1/2 phosphorylation. U0126, at 30 mum, that blocks ERK1/2 signaling selectively attenuated neurite outgrowth induced by NGF and Bt(2)cAMP, but BIX02188 and BIX02189, at 30 mum, that block ERK5 signaling and an ERK5 dominant-negative mutant suppressed only NGF-induced neurite outgrowth. Next, we examined the expression of tyrosine hydroxylase, a rate-limiting enzyme of catecholamine biosynthesis. Both NGF and Bt(2)cAMP increased tyrosine hydroxylase gene promoter activity in an ERK1/2-dependent manner but was ERK5-independent. However, when both ERK5 and ERK1/2 signalings were inhibited, tyrosine hydroxylase protein up-regulation by NGF and Bt(2)cAMP was abolished, because of the loss of stabilization of tyrosine hydroxylase protein by ERK5. Taking these results together, ERK5 is involved in neurite outgrowth and stabilization of tyrosine hydroxylase in PC12 cells, and ERK5, along with ERK1/2, plays essential roles in the neural differentiation process.

Indexed as

NeurogenesisAnimalsMitogen-Activated Protein Kinase 7Nerve Growth FactorNeuritesPC12 CellsPhosphorylationRatsSignal TransductionTyrosine 3-MonooxygenaseMitogen-Activated Protein Kinase 7Nerve Growth FactorTyrosine 3-Monooxygenase

Identifiers

PMID19581298
PMCPMC2749131
OpenAlexW2041502163

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.