Evidence map›Paper›PMID 18925939›Full record

ArticleNeural development2008

Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth.

Pei-I Tsai, Hsiu-Hua Kao, Caroline Grabbe, Yu-Tao Lee, Aurnab Ghose, Tzu-Ting Lai, Kuan-Po Peng, David Van Vactor, Ruth H Palmer, Ruey-Hwa Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Neural development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  11. The Spacing Effect for Structural Synaptic Plasticity Provides Specificity and Precision in Plastic Changes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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  13. Activity-Induced Synaptic Structural Modifications by an Activator of Integrin Signaling at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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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

12 authors at 6 institutions in 4 countries.

Pei-I TsaiInstitute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan. newchris@gate.sinica.edu.tw
Hsiu-Hua Kao
Caroline Grabbe
Yu-Tao Lee
Aurnab Ghose
Tzu-Ting Lai
Kuan-Po Peng
David Van Vactor
Ruth H Palmer
Ruey-Hwa Chen
Shih-Rung Yeh
Cheng-Ting Chien
Institute of Molecular Biology, Academia Sinica · TWNational Tsing Hua University · TWUmeå University · SEHarvard University · USIndian Institute of Science Education and Research Pune · INNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFocal adhesion kinase (FAK) functions in cell migration and signaling through activation of the mitogen-activated protein kinase (MAPK) signaling cascade. Neuronal function of FAK has been suggested to control axonal branching; however, the underlying mechanism in this process is not clear.

resultsWe have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin alphaPS3betanu heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity.

conclusionWe conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes.

Indexed as

AnimalsDown-RegulationDrosophilaDrosophila ProteinsElectrophysiologyFocal Adhesion Kinase 1ImmunohistochemistryIntegrin beta ChainsMicroscopy, ConfocalMitogen-Activated Protein KinasesMutationNeuromuscular JunctionPhosphorylationProto-Oncogene Proteins pp60(c-src)Signal TransductionSynaptic PotentialsDrosophila ProteinsFak protein, DrosophilaFocal Adhesion Kinase 1Integrin beta Chainsintegrin betanu, DrosophilaMitogen-Activated Protein KinasesProto-Oncogene Proteins pp60(c-src)Src42A protein, Drosophila

Identifiers

PMID18925939
PMCPMC2576229
OpenAlexW2119274752

What OpenQuestion holds

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Registered trials

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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.