Evidence map›Paper›PMID 15672554›Full record

ArticleNeurochemical research2004

Role of MAPK/ERK in neurotrophin-4 potentiation of necrotic neuronal death.

Doug Lobner, Geraldine Liot

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 52% 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

6 citing papers in PubMed, 16 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

2 authors at 2 institutions in 2 countries.

Doug LobnerDepartment of Biomedical Sciences, Marquette University, Milwaukee, WI 53233, USA. Doug.Lobner@marquette.edu
Geraldine Liot
Centre National de la Recherche Scientifique · FRMarquette University · US

Funding

MECHANISMS OF INJURY POTENTIATION BY GROWTH FACTORSR01AG016708 · NIA · MARQUETTE UNIVERSITY · PI LOBNER, DOUGLAS C · 2000 to 2004
$1.0M
NIA NIH HHS AG16708
6 · The paper itself

Abstract

Neurotrophic factors have been proposed for the treatment of a variety of neurological diseases. However, to this point they have failed in clinical trials. One potential problem is that while neurotrophic factors attenuate apoptosis, they have the potential to enhance necrosis. In this study we show that neurotrophin-4 (NT-4) attenuated apoptotic neuronal death while potentiating necrotic neuronal death in cortical cultures. The protective effects of NT-4 were not blocked by the mitogen-activated protein kinase kinase (MEK) inhibitors PD098059 or U0126, while the injury potentiation by NT-4 was blocked by these inhibitors. NT-4 stimulated the phosphorylation of ERK1/2 and this phosphorylation was attenuated by U0126 and PD098059. The results indicate a disassociation between the pathway by which NT-4 potentiates necrosis, and that by which it attenuates apoptosis, and suggest that addition of a MEK inhibitor may enhance the beneficial effects of NT-4 in treating complex injuries such as occur in vivo.

Indexed as

AnimalsButadienesCell DeathCells, CulturedCyclosporineEnzyme ActivationFlavonoidsImmunosuppressive AgentsL-Lactate DehydrogenaseMiceMitogen-Activated Protein KinasesNecrosisNerve Growth FactorsNeuronsNitrilesPhosphorylation2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneButadienesCyclosporineFlavonoidsImmunosuppressive AgentsL-Lactate DehydrogenaseMitogen-Activated Protein KinasesNerve Growth Factorsneurotrophin 4NitrilesTetrazolium SaltsThiazolesthiazolyl blueU 0126

Identifiers

PMID15672554
OpenAlexW2039851720

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.