ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
LMTK3 deficiency causes pronounced locomotor hyperactivity and impairs endocytic trafficking.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Article
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- Multimodal analysis of cell-free DNA identifies epigenetic biomarkers for amyotrophic lateral sclerosis diagnosis and progression.bioRxiv : the preprint server for biology · 2026Article
- Exploiting O-GlcNAc dyshomeostasis to screen O-GlcNAc transferase intellectual disability variants.Stem cell reports · 2025Article
- Brain Specific RagA Overexpression Triggers Depressive-Like Behaviors in Mice via Activating ADORA2A Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The lemur tail kinase family in neuronal function and disfunction in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- The brain-specific kinase LMTK3 regulates neuronal excitability by decreasing KCC2-dependent neuronal CliScience · 2024Article
- VBASS enables integration of single cell gene expression data in Bayesian association analysis of rare variants.Communications biology · 2023Article
- TOB is an effector of the hippocampus-mediated acute stress response.Translational psychiatry · 2022Article
- The multifaceted role of lemur tyrosine kinase 3 in health and disease.Open biology · 2021Review
- Hyperactive and impulsive behaviors of LMTK1 knockout mice.Scientific reports · 2020Article
- LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons.Frontiers in molecular neuroscience · 2020Article
- Acquired Expression of MutantThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Cocaine Self-administration Alters Transcriptome-wide Responses in the Brain's Reward Circuitry.Biological psychiatry · 2018Article
- Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression.Science signaling · 2017Article
- Phosphorylation of Rab-coupling protein by LMTK3 controls Rab14-dependent EphA2 trafficking to promote cell:cell repulsion.Nature communications · 2017Article
- Whole Genome Duplications Shaped the Receptor Tyrosine Kinase Repertoire of Jawed Vertebrates.Genome biology and evolution · 2016Article
- Emerging roles of ARHGAP33 in intracellular trafficking of TrkB and pathophysiology of neuropsychiatric disorders.Nature communications · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LMTK3 belongs to the LMTK family of protein kinases that are predominantly expressed in the brain. Physiological functions of LMTK3 and other members of the LMTK family in the CNS remain unknown. In this study, we performed a battery of behavioral analyses using Lmtk3(-/-) mice and showed that these mice exhibit abnormal behaviors, including pronounced locomotor hyperactivity, reduced anxiety behavior, and decreased depression-like behavior. Concurrently, the dopamine metabolite levels and dopamine turnover rate are increased in the striata of Lmtk3(-/-) mice compared with wild-type controls. In addition, using cultured primary neurons from Lmtk3(-/-) mice, we found that LMTK3 is involved in the endocytic trafficking of N-methyl-d-aspartate receptors, a type of ionotropic glutamate receptor. Altered membrane traffic of the receptor in Lmtk3(-/-) neurons may underlie behavioral abnormalities in the mutant animals. Together, our data suggest that LMTK3 plays an important role in regulating locomotor behavior in mice.
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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.