Evidence map›Paper›PMID 31628178›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

The LMTK1-TBC1D9B-Rab11A Cascade Regulates Dendritic Spine Formation via Endosome Trafficking.

Hironori Nishino, Taro Saito, Ran Wei, Tetsuya Takano, Koji Tsutsumi, Makoto Taniguchi, Kanae Ando, Mineko Tomomura, Mitsunori Fukuda, Shin-Ichi Hisanaga

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. The Recycling Endosomal (NaActa physiologica (Oxford, England) · 2026
    Article
  3. Restoration neurite growth by removing the blockage of endosome trafficking in Alzheimer-like mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Review
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  12. Review
  13. A Novel Constitutively ActiveHuman mutation · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022
    Review
  18. Article
  19. Review
  20. Article
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 4 institutions in 2 countries.

Hironori NishinoDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.ORCID 0000-0001-8573-9899
Taro SaitoDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Ran WeiDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Tetsuya TakanoDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Koji TsutsumiDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Makoto TaniguchiDepartment of Neuroscience, Medical University of South Carolina, Charleston, South Carolina 29425.
Kanae AndoDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Mineko TomomuraDepartment of Oral Health Sciences, Meikai University School of Dentistry, Urayasu, Chiba 279-9950, Japan, and.
Mitsunori FukudaDepartment of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Aoba-ku, Sendai, Miyagi 980-8578, Japan.ORCID 0000-0002-8620-5853
Shin-Ichi HisanagaDepartment of Biological Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan, hisanaga-shinichi@tmu.ac.jp.ORCID 0000-0002-7572-472X
Tokyo Metropolitan University · JPMedical University of South Carolina · USMeikai University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic spines are postsynaptic protrusions at excitatory synapses that are critical for proper neuronal synaptic transmission. While lipid and protein membrane components are necessary for spine formation, it is largely unknown how they are recruited to developing spines. Endosomal trafficking is one mechanism that may influence this development. We recently reported that Lemur kinase 1A (LMTK1A), a membrane-bound Ser/Thr kinase, regulates trafficking of endosomes in neurons. LMTK1 has been shown to be a p35 Cdk5 activator-binding protein and a substrate for Cdk5-p35; however, its neuronal function has not been sufficiently studied. Here, we investigate the role of LMTK1 in spine formation. Depletion of LMTK1 increases spine formation, maturation, and density in primary cultured neurons and in mouse brain of either sex. Additionally, expression of kinase-negative LMTK1 stimulates spine formation in primary neurons and

Indexed as

AnimalsApoptosis Regulatory ProteinsChlorocebus aethiopsCOS CellsDendritic SpinesEndosomesFemaleHEK293 CellsHippocampusHumansMiceMice, Inbred ICRMice, KnockoutPregnancyProtein TransportProtein-Tyrosine KinasesAatk protein, mouseApoptosis Regulatory ProteinsProtein-Tyrosine Kinasesrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsTBC1D9 protein, mouseCdk5endosomeGAPmembrane traffickingRabspine

Identifiers

PMID31628178
PMCPMC6880470
OpenAlexW2980851272

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.