Evidence map›Paper›PMID 29631601›Full record

ReviewMolecular brain2018

Biological function of Lemur tyrosine kinase 2 (LMTK2): implications in neurodegeneration.

János Bencze, Gábor Miklós Mórotz, Woosung Seo, Viktor Bencs, János Kálmán, Christopher Charles John Miller, Tibor Hortobágyi

Open access · goldAbstract readReview
In one paragraph

Review in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. LMTK2 and CRB1 are two novel risk genes for Alzheimer's disease in Han Chinese.The journal of prevention of Alzheimer's disease · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Lemur Tyrosine Kinases and Prostate Cancer: A Literature Review.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons.Frontiers in molecular neuroscience · 2020
    Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

János BenczeDivision of Neuropathology, Institute of Pathology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., Debrecen, H-4032, Hungary.
Gábor Miklós MórotzDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry Psychology and Neuroscience, King's College London, London, UK.
Woosung SeoDivision of Neuropathology, Institute of Pathology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., Debrecen, H-4032, Hungary.
Viktor BencsDivision of Neuropathology, Institute of Pathology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., Debrecen, H-4032, Hungary.
János KálmánDepartment of Psychiatry, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Christopher Charles John MillerDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry Psychology and Neuroscience, King's College London, London, UK.
Tibor HortobágyiDivision of Neuropathology, Institute of Pathology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., Debrecen, H-4032, Hungary. tibor.hortobagyi@kcl.ac.uk.
University of Debrecen · HUKing's College London · GBUniversity of Szeged · HU

Funding

Biotechnology and Biological Sciences Research Council BB/L019299/1Emberi Eroforrások Minisztériuma EFOP-3.6.3-VEKOP-16-2017-00009Emberi Eroforrások Minisztériuma ÚNKP-17-3Magyarország Kormánya GINOP-2.3.2-15-2016-00043Magyar Tudományos Akadémia 2017-1.2.1-NKP-2017-00002Magyar Tudományos Akadémia KTIA_NAP_13-1-2013-0001
6 · The paper itself

Abstract

Neurodegenerative disorders are frequent, incurable diseases characterised by abnormal protein accumulation and progressive neuronal loss. Despite their growing prevalence, the underlying pathomechanism remains unclear. Lemur tyrosine kinase 2 (LMTK2) is a member of a transmembrane serine/threonine-protein kinase family. Although it was described more than a decade ago, our knowledge on LMTK2's biological functions is still insufficient. Recent evidence has suggested that LMTK2 is implicated in neurodegeneration. After reviewing the literature, we identified three LMTK2-mediated mechanisms which may contribute to neurodegenerative processes: disrupted axonal transport, tau hyperphosphorylation and enhanced apoptosis. Moreover, LMTK2 gene expression is decreased in an Alzheimer's disease mouse model. According to these features, LMTK2 might be a promising therapeutic target in near future. However, further investigations are required to clarify the exact biological functions of this unique protein.

Indexed as

AnimalsApoptosisAxonal TransportHumansModels, BiologicalNerve DegenerationProtein BindingProtein Serine-Threonine KinasesProtein Serine-Threonine KinasesAlzheimer’s diseaseAxonal transportLMTK2NeurodegenerationTau

Identifiers

PMID29631601
PMCPMC5891947
OpenAlexW2796493152

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.