Evidence map›Paper›PMID 35121636›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022

SIPA1L1/SPAR1 Interacts with the Neurabin Family of Proteins and is Involved in GPCR Signaling.

Ken Matsuura, Shizuka Kobayashi, Kohtarou Konno, Miwako Yamasaki, Takahiro Horiuchi, Takao Senda, Tomoatsu Hayashi, Kiyotoshi Satoh, Fumiko Arima-Yoshida, Kei Iwasaki and 10 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.6field-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

13 citing papers in PubMed, 25 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

20 authors at 6 institutions in 2 countries.

Ken MatsuuraLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan ken.matsuura@oist.jp akiyama@iqb.u-tokyo.ac.jp.ORCID 0000-0003-0247-3867
Shizuka KobayashiDivision of Neuronal Network, Department of Basic Medical Sciences, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.ORCID 0000-0002-2138-1231
Kohtarou KonnoDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Miwako YamasakiDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Takahiro HoriuchiLaboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Takao SendaDepartment of Anatomy, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan.
Tomoatsu HayashiLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Kiyotoshi SatohLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Fumiko Arima-YoshidaDivision of Neuronal Network, Department of Basic Medical Sciences, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
Kei IwasakiLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Lumi NegishiLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Naomi Yasui-ShimizuLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Kazuyoshi KohuLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Shigenori KawaharaLaboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0002-7716-6442
Yutaka KirinoLaboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Tsutomu NakamuraLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan.
Masahiko WatanabeDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.ORCID 0000-0001-5037-7138
Tadashi YamamotoCell Signal Unit, Okinawa Institute of Science and Technology, Onna-son 904-0495, Japan.
Toshiya ManabeDivision of Neuronal Network, Department of Basic Medical Sciences, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
Tetsu AkiyamaLaboratory of Molecular and Genetic Information, Institute for Quantitative Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0032, Japan ken.matsuura@oist.jp akiyama@iqb.u-tokyo.ac.jp.
Quantitative BioSciences · USThe University of Tokyo · JPHokkaido University · JPOkinawa Institute of Science and Technology Graduate University · JPGifu University · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal-induced proliferation-associated 1 (SIPA1)-like 1 (SIPA1L1; also known as SPAR1) has been proposed to regulate synaptic functions that are important in maintaining normal neuronal activities, such as regulating spine growth and synaptic scaling, as a component of the PSD-95/NMDA-R-complex. However, its physiological role remains poorly understood. Here, we performed expression analyses using super-resolution microscopy (SRM) in mouse brain and demonstrated that SIPA1L1 is mainly localized to general submembranous regions in neurons, but surprisingly, not to PSD. Our screening for physiological interactors of SIPA1L1 in mouse brain identified spinophilin and neurabin-1, regulators of G-protein-coupled receptor (GPCR) signaling, but rejected PSD-95/NMDA-R-complex components. Furthermore,

Indexed as

Nerve Tissue ProteinsN-MethylaspartateAnimalsDisks Large Homolog 4 ProteinGTPase-Activating ProteinsMaleMiceMice, KnockoutMicrofilament ProteinsNeurabinsReceptor, Adenosine A1Receptors, G-Protein-CoupledDisks Large Homolog 4 ProteinGTPase-Activating ProteinsMicrofilament ProteinsNerve Tissue ProteinsNeurabinsN-MethylaspartateReceptor, Adenosine A1Receptors, G-Protein-CoupledSipa1l1 protein, mouseGPCRneurabinPSDSIPA1L1SPARspinophilin

Identifiers

PMID35121636
PMCPMC8944240
OpenAlexW4210290038

What Socratic 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 Socratic graph.