Evidence map›Paper›PMID 26717414›Full record

ArticlePloS one2015

Heterozygous Disruption of Autism susceptibility candidate 2 Causes Impaired Emotional Control and Cognitive Memory.

Kei Hori, Taku Nagai, Wei Shan, Asami Sakamoto, Manabu Abe, Maya Yamazaki, Kenji Sakimura, Kiyofumi Yamada, Mikio Hoshino

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Cells · 2022
    Article
  13. The HDAC inhibitor CI-994 acts as a molecular memory aid by facilitating synaptic and intracellular communication after learning.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Review
  15. AUTS2 Syndrome: Molecular Mechanisms and Model Systems.Frontiers in molecular neuroscience · 2022
    Review
  16. Cells · 2021
    Review
  17. Review
  18. Review
  19. Article
  20. Comparing a Novel Malformation Syndrome Caused by Pathogenic Variants inFrontiers in cell and developmental biology · 2021
    Review
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

9 authors at 3 institutions in 1 country.

Kei HoriDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Taku NagaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Wei ShanDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Asami SakamotoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Manabu AbeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Maya YamazakiDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Kiyofumi YamadaDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Mikio HoshinoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Nagoya University Hospital · JPNational Center of Neurology and Psychiatry · JPNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the Autism susceptibility candidate 2 gene (AUTS2) have been associated with a broad range of psychiatric illnesses including autism spectrum disorders, intellectual disability and schizophrenia. We previously demonstrated that the cytoplasmic AUTS2 acts as an upstream factor for the Rho family small GTPase Rac1 and Cdc42 that regulate the cytoskeletal rearrangements in neural cells. Moreover, genetic ablation of the Auts2 gene in mice has resulted in defects in neuronal migration and neuritogenesis in the developing cerebral cortex caused by inactivation of Rac1-signaling pathway, suggesting that AUTS2 is required for neural development. In this study, we conducted a battery of behavioral analyses on Auts2 heterozygous mutant mice to examine the involvement of Auts2 in adult cognitive brain functions. Auts2-deficient mice displayed a decrease in exploratory behavior as well as lower anxiety-like behaviors in the absence of any motor dysfunction. Furthermore, the capability for novel object recognition and cued associative memory were impaired in Auts2 mutant mice. Social behavior and sensory motor gating functions were, however, normal in the mutant mice as assessed by the three-chamber test and prepulse inhibition test, respectively. Together, our findings indicate that AUTS2 is critical for the acquisition of neurocognitive function.

Indexed as

EmotionsGenetic Association StudiesHeterozygoteMemoryMutationAnimalsAnxietyBehavior, AnimalBrainCognitionCytoskeletal ProteinsFemaleMaleMiceModels, AnimalProteinsAUTS2 protein, humanCytoskeletal ProteinsProteinsTranscription Factors

Identifiers

PMID26717414
PMCPMC4699902
OpenAlexW2219431323

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.