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Publications by authors named "Ryota Nagatomo"

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Soluble form of Lingo2, an autism spectrum disorder-associated molecule, functions as an excitatory synapse organizer in neurons.
Fumiaki Yoshida Ryota Nagatomo Shun Utsunomiya Misaki Kimura Shiyori Shun

Transl Psychiatry

October 2024

Article Synopsis
  • * Research identified that levels of Lingo2, a protein linked to excitatory synapse formation, were increased in neurons from the VPA model, suggesting its role as an excitatory synapse organizer.
  • * The secreted form of Lingo2 (sLingo2) was found to enhance excitatory synapses in both mouse and human neurons, indicating that better understanding sLingo2's mechanisms could shed light on the development of ASD.
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Autism-associated variants of neuroligin 4X impair synaptogenic activity by various molecular mechanisms.
Takafumi Yumoto Misaki Kimura Ryota Nagatomo Tsukika Sato Shun Utsunomiya

Mol Autism

September 2020

Background: Several genetic alterations, including point mutations and copy number variations in NLGN genes, have been associated with psychiatric disorders, such as autism spectrum disorder (ASD) and X-linked mental retardation (XLMR). NLGN genes encode neuroligin (NL) proteins, which are adhesion molecules that are important for proper synaptic formation and maturation. Previously, we and others found that the expression level of murine NL1 is regulated by proteolytic processing in a synaptic activity-dependent manner.

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Synopsis of recent research by authors named "Ryota Nagatomo"

  • - Ryota Nagatomo's research primarily focuses on the molecular mechanisms underlying Autism Spectrum Disorder (ASD), particularly the roles of synaptic proteins such as Lingo2 and neuroligins in neuronal function and behavior.
  • - His 2024 study on the soluble form of Lingo2 demonstrates its function as an excitatory synapse organizer in impaired models of ASD, revealing potential therapeutic targets for correcting synaptic imbalances.
  • - In an earlier 2020 publication, he examined how autism-associated variants of neuroligin 4X disrupt synaptogenic activity through various mechanisms, emphasizing the significance of NLGN gene alterations in the pathology of ASD and related disorders.

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