Evidence map›Paper›PMID 16000625›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Constitutively active cytoplasmic c-Jun N-terminal kinase 1 is a dominant regulator of dendritic architecture: role of microtubule-associated protein 2 as an effector.

Benny Björkblom, Nina Ostman, Vesa Hongisto, Vladislav Komarovski, Jan-Jonas Filén, Tuula A Nyman, Tuula Kallunki, Michael J Courtney, Eleanor T Coffey

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

91 citing papers in PubMed, 181 citations in OpenAlex.

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  8. DualInternational journal of molecular sciences · 2021
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  18. JNK Regulation of Depression and Anxiety.Brain plasticity (Amsterdam, Netherlands) · 2018
    Review
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 2 countries.

Benny BjörkblomTurku Centre for Biotechnology, Abo Akademi and Turku University, BioCity, FIN-20521 Turku, Finland.
Nina Ostman
Vesa Hongisto
Vladislav Komarovski
Jan-Jonas Filén
Tuula A Nyman
Tuula Kallunki
Michael J Courtney
Eleanor T Coffey
Turku Centre for Biotechnology · FIUniversity of Eastern Finland · FIÅbo Akademi University · FIDanish Cancer Society · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal functioning of the nervous system requires precise regulation of dendritic shape and synaptic connectivity. Here, we report a severe impairment of dendritic structures in the cerebellum and motor cortex of c-Jun N-terminal kinase 1 (JNK1)-deficient mice. Using an unbiased screen for candidate mediators, we identify the dendrite-specific high-molecular-weight microtubule-associated protein 2 (MAP2) as a JNK substrate in the brain. We subsequently show that MAP2 is phosphorylated by JNK in intact cells and that MAP2 proline-rich domain phosphorylation is decreased in JNK1-/- brain. We developed compartment-targeted JNK inhibitors to define whether a functional relationship exists between the physiologically active, cytosolic pool of JNK and dendritic architecture. Using these, we demonstrate that cytosolic, but not nuclear, JNK determines dendritic length and arbor complexity in cultured neurons. Moreover, we confirm that MAP2-dependent process elongation is enhanced after activation of JNK. Using JNK1-/- neurons, we reveal a dominant role for JNK1 over ERK in regulating dendritic arborization, whereas ERK only regulates dendrite shape under conditions in which JNK activity is low (JNK1-/- neurons). These results reveal a novel antagonism between JNK and ERK, potentially providing a mechanism for fine-tuning the dendritic arbor. Together, these data suggest that JNK phosphorylation of MAP2 plays an important role in defining dendritic architecture in the brain.

Indexed as

AnimalsCell DifferentiationCell NucleusCells, CulturedCerebellar CortexChlorocebus aethiopsCOS CellsCytosolDendritesMiceMice, KnockoutMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 8Motor CortexMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 8Recombinant Fusion Proteins

Identifiers

PMID16000625
PMCPMC6725281
OpenAlexW2045562863

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.