Evidence map›Paper›PMID 27852895›Full record

ArticleMolecular biology of the cell2017

Ras and Rab interactor 1 controls neuronal plasticity by coordinating dendritic filopodial motility and AMPA receptor turnover.

Zsófia Szíber, Hanna Liliom, Carlos O Oueslati Morales, Attila Ignácz, Anikó Erika Rátkai, Kornelia Ellwanger, Gisela Link, Attila Szűcs, Angelika Hausser, Katalin Schlett

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  12. Mechanisms of AMPA Receptor Endosomal Sorting.Frontiers in molecular neuroscience · 2018
    Review
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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

10 authors at 2 institutions in 2 countries.

Zsófia SzíberDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Hanna LiliomDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Carlos O Oueslati MoralesInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Attila IgnáczDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Anikó Erika RátkaiDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Kornelia EllwangerInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Gisela LinkInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Attila SzűcsMTA-ELTE-NAP B Neuronal Cell Biology Research Group, H-1117 Budapest, Hungary.
Angelika HausserInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Katalin SchlettDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary schlett.katalin@ttk.elte.hu.
Eötvös Loránd University · HUUniversity of Stuttgart · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras and Rab interactor 1 (RIN1) is predominantly expressed in the nervous system. RIN1-knockout animals have deficits in latent inhibition and fear extinction in the amygdala, suggesting a critical role for RIN1 in preventing the persistence of unpleasant memories. At the molecular level, RIN1 signals through Rab5 GTPases that control endocytosis of cell-surface receptors and Abl nonreceptor tyrosine kinases that participate in actin cytoskeleton remodeling. Here we report that RIN1 controls the plasticity of cultured mouse hippocampal neurons. Our results show that RIN1 affects the morphology of dendritic protrusions and accelerates dendritic filopodial motility through an Abl kinase-dependent pathway. Lack of RIN1 results in enhanced mEPSC amplitudes, indicating an increase in surface AMPA receptor levels compared with wild-type neurons. We further provide evidence that the Rab5 GEF activity of RIN1 regulates surface GluA1 subunit endocytosis. Consequently loss of RIN1 blocks surface AMPA receptor down-regulation evoked by chemically induced long-term depression. Our findings indicate that RIN1 destabilizes synaptic connections and is a key player in postsynaptic AMPA receptor endocytosis, providing multiple ways of negatively regulating memory stabilization during neuronal plasticity.

Indexed as

AnimalsCell MovementDendritesEndocytosisHippocampusIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityNeuronsProto-Oncogene Proteins c-ablPseudopodiarab5 GTP-Binding Proteinsrab GTP-Binding ProteinsReceptors, AMPAIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-ablrab5 GTP-Binding Proteinsrab GTP-Binding ProteinsReceptors, AMPARin1 protein, mouse

Identifiers

PMID27852895
PMCPMC5231897
OpenAlexW2554526564

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.