OSCR

Targeting notch signaling to restore neural development and behavior in mouse models of ASD.

Overview

Authors: Yoko Hanno1,2, Moe Nakanishi3, Akinori Takase4, Jun Nomura5, Masami Tanaka1, Yumi Iida4, Masayuki Tanaka4, Hiroyuki Hosokawa6, Masatoshi Ito7, Katsunaka Mikami8, Katsuto Hozumi6, Goichi Miyoshi9, Toru Takumi3,5, Takatoshi Iijima1,10
  1. Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa Japan
  2. Present Address: Laboratory for Neural Cell Dynamics, RIKEN Center for Brain Science, Saitama, Japan
  3. RIKEN Center for Brain Science, Wako, Saitama, Japan
  4. The Support Center for Medical Research and Education, Tokai University, Isehara, Kanagawa Japan
  5. Department of Physiology and Cell Biology, Kobe University School of Medicine, Chuo, Kobe, Japan
  6. Department of Immunology, Tokai University School of Medicine, Isehara, Kanagawa Japan
  7. Department of Legal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa Japan
  8. Department of Psychiatry, Tokai University School of Medicine, Isehara, Kanagawa Japan
  9. Department of Developmental Genetics and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Gunma, Japan
  10. Present Address: Department of Anatomy, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa Japan
Journal: Nature communications, volume 17, issue 1, article 2587
Dates: received 16 April 2025; accepted 23 February 2026; published online 30 March 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1038/s41467-026-70321-6 · PMID 41912527 · PMCID PMC13036009 · OpenAlex W7143442819
Open access: gold, a free copy (OpenAlex)
Categories: human (organism), mouse (organism), autism (population)
Methods: Preprocessing, Statistics, Smoothing, state filtering, decompositions, Connectivity, Machine learning
Keywords: Autism spectrum disorders, Epigenetics and behaviour, Social behaviour, Cell fate and cell lineage
MeSH: Autism Spectrum Disorder*, Neurogenesis*, Receptor, Notch1*, Receptor, Notch2*, Receptors, Notch*, Amyloid Precursor Protein Secretases, Animals, Behavior, Animal, Disease Models, Animal, Epigenesis, Genetic, Female, GABAergic Neurons, Ganglionic Eminence, Humans, Interneurons, Male, Mice, Neurodevelopment, Signal Transduction, Vasoactive Intestinal Peptide (* major topic)
Topic: Neurogenesis and neuroplasticity mechanisms (Developmental Neuroscience, Neuroscience), according to OpenAlex
Funding: MEXT | Japan Society for the Promotion of Science (21K07327, 20K22913, 24K10716, 15K14355)
Citations: cited by 1 paper (Europe PMC); 70 references in the paper

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

Code

The paper links to its data and to no code of its authors: see the Data section.

Code availability statement

The paper has a code availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

  • no repository, dataset or request procedure was recognized in it

Read it in the paper: doi.org/10.1038/s41467-026-70321-6.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Code and data availability statement

The paper has a code and data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

Read it in the paper: doi.org/10.1038/s41467-026-70321-6.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 14 authors, 4 keywords, 20 MeSH terms, 1 funder, 70 references.

Cite

This paper

Hanno, Y., Nakanishi, M., Takase, A., Nomura, J., Tanaka, M., Iida, Y., Tanaka, M., Hosokawa, H., Ito, M., Mikami, K., Hozumi, K., Miyoshi, G., Takumi, T., & Iijima, T. (2026). Targeting notch signaling to restore neural development and behavior in mouse models of ASD. Nature communications, 17(1), 2587. https://doi.org/10.1038/s41467-026-70321-6

BibTeX

@article{hanno2026targeting,
author = {Hanno, Yoko and Nakanishi, Moe and Takase, Akinori and Nomura, Jun and Tanaka, Masami and Iida, Yumi and Tanaka, Masayuki and Hosokawa, Hiroyuki and Ito, Masatoshi and Mikami, Katsunaka and Hozumi, Katsuto and Miyoshi, Goichi and Takumi, Toru and Iijima, Takatoshi},
title = {{Targeting notch signaling to restore neural development and behavior in mouse models of ASD}},
journal = {Nature communications},
year = {2026},
month = mar,
volume = {17},
number = {1},
pages = {2587},
publisher = {Nature Publishing Group},
issn = {2041-1723},
doi = {10.1038/s41467-026-70321-6},
url = {https://doi.org/10.1038/s41467-026-70321-6},
pmid = {41912527},
pmcid = {PMC13036009}
}

RIS

TY - JOUR
AU - Hanno, Yoko
AU - Nakanishi, Moe
AU - Takase, Akinori
AU - Nomura, Jun
AU - Tanaka, Masami
AU - Iida, Yumi
AU - Tanaka, Masayuki
AU - Hosokawa, Hiroyuki
AU - Ito, Masatoshi
AU - Mikami, Katsunaka
AU - Hozumi, Katsuto
AU - Miyoshi, Goichi
AU - Takumi, Toru
AU - Iijima, Takatoshi
TI - Targeting notch signaling to restore neural development and behavior in mouse models of ASD
T2 - Nature communications
J2 - Nat Commun
PY - 2026
DA - 2026/03/30
VL - 17
IS - 1
SP - 2587
SN - 2041-1723
PB - Nature Publishing Group
DO - 10.1038/s41467-026-70321-6
UR - https://doi.org/10.1038/s41467-026-70321-6
LA - en
ER -

CSL-JSON

{
"id": "10.1038/s41467-026-70321-6",
"type": "article-journal",
"title": "Targeting notch signaling to restore neural development and behavior in mouse models of ASD",
"container-title": "Nature communications",
"author": [
{
"family": "Hanno",
"given": "Yoko"
},
{
"family": "Nakanishi",
"given": "Moe"
},
{
"family": "Takase",
"given": "Akinori"
},
{
"family": "Nomura",
"given": "Jun"
},
{
"family": "Tanaka",
"given": "Masami"
},
{
"family": "Iida",
"given": "Yumi"
},
{
"family": "Tanaka",
"given": "Masayuki"
},
{
"family": "Hosokawa",
"given": "Hiroyuki"
},
{
"family": "Ito",
"given": "Masatoshi"
},
{
"family": "Mikami",
"given": "Katsunaka"
},
{
"family": "Hozumi",
"given": "Katsuto"
},
{
"family": "Miyoshi",
"given": "Goichi"
},
{
"family": "Takumi",
"given": "Toru"
},
{
"family": "Iijima",
"given": "Takatoshi"
}
],
"container-title-short": "Nat Commun",
"volume": "17",
"issue": "1",
"page": "2587",
"DOI": "10.1038/s41467-026-70321-6",
"PMID": "41912527",
"PMCID": "PMC13036009",
"ISSN": "2041-1723",
"publisher": "Nature Publishing Group",
"URL": "https://doi.org/10.1038/s41467-026-70321-6",
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
30
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.3389/fncel.2024.1414955
Genetic approaches to elucidating cortical and hippocampal GABAergic interneuron diversity.
Journal: Frontiers in cellular neuroscience
In common: portal.brain-map.org/atlases-and-data/rnaseq, 6 references
[2] doi:10.3389/fncir.2022.982721
Cell-type specific transcriptomic signatures of neocortical circuit organization and their relevance to autism.
Journal: Frontiers in neural circuits
In common: portal.brain-map.org/atlases-and-data/rnaseq, autism, mouse, 5 references
[3] doi:10.1073/pnas.2317783121
Developmental trajectories of GABAergic cortical interneurons are sequentially modulated by dynamic <i>FoxG1</i> expression levels.
Journal: Proceedings of the National Academy of Sciences of the United States of America
In common: mouse, 3 references, author Goichi Miyoshi
[4] doi:10.1038/s41380-024-02479-8
Transcriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor.
Journal: Molecular psychiatry
In common: autism, mouse, 1 reference, author Toru Takumi
[5] doi:10.1038/s41467-025-67930-y
Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice.
Journal: Nature communications
In common: portal.brain-map.org/atlases-and-data/rnaseq, autism, mouse, 2 references
[6] doi:10.1186/s12974-024-03100-z
Maternal immunoglobulin G affects brain development of mouse offspring.
Journal: Journal of neuroinflammation
In common: mouse, 1 reference, author Takatoshi Iijima
[7] doi:10.1113/jp286439
Inhibition of BK channels by GABAb receptors enhances intrinsic excitability of layer 2/3 vasoactive intestinal polypeptide-expressing interneurons in mouse neocortex.
Journal: The Journal of physiology
In common: mouse, 4 references
[8] doi:10.1186/s13229-023-00557-2 [code]
Shank3 deletion in PV neurons is associated with abnormal behaviors and neuronal functions that are rescued by increasing GABAergic signaling.
Journal: Molecular autism
In common: autism, mouse, 4 references
[9] doi:10.7554/elife.85893 [code]
Id2 GABAergic interneurons comprise a neglected fourth major group of cortical inhibitory cells.
Journal: eLife
In common: portal.brain-map.org/atlases-and-data/rnaseq, mouse, 2 references
[10] doi:10.1038/s12276-024-01386-w
The WAVE complex in developmental and adulthood brain disorders.
Journal: Experimental & molecular medicine
In common: portal.brain-map.org/atlases-and-data/rnaseq, autism, 2 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: code errors and mismatches between the code and the paper about this paper and its code, from readers and its authors, beside the paper and its tracing map.

Reproductions: reports from readers who ran the authors' code and did not get the paper's result, what they ran, with which environment, commit and data.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.