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Hyperactive and impulsive behaviors of LMTK1 knockout mice
Lemur tail kinase 1 (LMTK1), previously called Apoptosis-Associated Tyrosine Kinase (AATYK), remains an uncharacterized Ser/Thr protein kinase that is predominantly expressed in the brain. It is recently reported that LMTK1A, an isoform of LMTK1, binds to recycling endosomes through its palmitoylati...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7508861/ https://www.ncbi.nlm.nih.gov/pubmed/32963255 http://dx.doi.org/10.1038/s41598-020-72304-z |
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author | Takahashi, Miyuki Sugiyama, Arika Wei, Ran Kobayashi, Shizuka Fukuda, Kimiko Nishino, Hironori Takahashi, Roka Tsutsumi, Koji Kita, Ichiro Ando, Kanae Manabe, Toshiya Kamiguchi, Hiroyuki Tomomura, Mineko Hisanaga, Shin-ichi |
author_facet | Takahashi, Miyuki Sugiyama, Arika Wei, Ran Kobayashi, Shizuka Fukuda, Kimiko Nishino, Hironori Takahashi, Roka Tsutsumi, Koji Kita, Ichiro Ando, Kanae Manabe, Toshiya Kamiguchi, Hiroyuki Tomomura, Mineko Hisanaga, Shin-ichi |
author_sort | Takahashi, Miyuki |
collection | PubMed |
description | Lemur tail kinase 1 (LMTK1), previously called Apoptosis-Associated Tyrosine Kinase (AATYK), remains an uncharacterized Ser/Thr protein kinase that is predominantly expressed in the brain. It is recently reported that LMTK1A, an isoform of LMTK1, binds to recycling endosomes through its palmitoylation and regulates endosomal trafficking by suppressing the activity of Rab11 small GTPase. In neurons, knockdown or knockout of LMTK1 results in longer axons, greater branching of dendrites and increased number of spines, suggesting that LMTK1 plays a role in neuronal circuit formation. However, its in vivo function remained to be investigated. Here, we examined the brain structures and behaviors of LMTK1 knockout (KO) mice. LMTK1 was expressed in most neurons throughout the brain. The overall brain structure appeared to be normal in LMTK1 KO mice, but the numbers of synapses were increased. LMTK1 KO mice had a slight impairment in memory formation and exhibited distinct psychiatric behaviors such as hyperactivity, impulsiveness and high motor coordination without social interaction deficits. Some of these abnormal behaviors represent core features of attention deficit hyperactive disorder (ADHD), suggesting the possible involvement of LMTK1 in the pathogenesis of ADHD. |
format | Online Article Text |
id | pubmed-7508861 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-75088612020-09-24 Hyperactive and impulsive behaviors of LMTK1 knockout mice Takahashi, Miyuki Sugiyama, Arika Wei, Ran Kobayashi, Shizuka Fukuda, Kimiko Nishino, Hironori Takahashi, Roka Tsutsumi, Koji Kita, Ichiro Ando, Kanae Manabe, Toshiya Kamiguchi, Hiroyuki Tomomura, Mineko Hisanaga, Shin-ichi Sci Rep Article Lemur tail kinase 1 (LMTK1), previously called Apoptosis-Associated Tyrosine Kinase (AATYK), remains an uncharacterized Ser/Thr protein kinase that is predominantly expressed in the brain. It is recently reported that LMTK1A, an isoform of LMTK1, binds to recycling endosomes through its palmitoylation and regulates endosomal trafficking by suppressing the activity of Rab11 small GTPase. In neurons, knockdown or knockout of LMTK1 results in longer axons, greater branching of dendrites and increased number of spines, suggesting that LMTK1 plays a role in neuronal circuit formation. However, its in vivo function remained to be investigated. Here, we examined the brain structures and behaviors of LMTK1 knockout (KO) mice. LMTK1 was expressed in most neurons throughout the brain. The overall brain structure appeared to be normal in LMTK1 KO mice, but the numbers of synapses were increased. LMTK1 KO mice had a slight impairment in memory formation and exhibited distinct psychiatric behaviors such as hyperactivity, impulsiveness and high motor coordination without social interaction deficits. Some of these abnormal behaviors represent core features of attention deficit hyperactive disorder (ADHD), suggesting the possible involvement of LMTK1 in the pathogenesis of ADHD. Nature Publishing Group UK 2020-09-22 /pmc/articles/PMC7508861/ /pubmed/32963255 http://dx.doi.org/10.1038/s41598-020-72304-z Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Takahashi, Miyuki Sugiyama, Arika Wei, Ran Kobayashi, Shizuka Fukuda, Kimiko Nishino, Hironori Takahashi, Roka Tsutsumi, Koji Kita, Ichiro Ando, Kanae Manabe, Toshiya Kamiguchi, Hiroyuki Tomomura, Mineko Hisanaga, Shin-ichi Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title | Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title_full | Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title_fullStr | Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title_full_unstemmed | Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title_short | Hyperactive and impulsive behaviors of LMTK1 knockout mice |
title_sort | hyperactive and impulsive behaviors of lmtk1 knockout mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7508861/ https://www.ncbi.nlm.nih.gov/pubmed/32963255 http://dx.doi.org/10.1038/s41598-020-72304-z |
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