Proteomics

Dataset Information

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Quantitative proteomic and phosphoproteomic profiling of Sh3rf3-deficient ASD mouse model via 6Plex-TMT and phosphoproteomic


ABSTRACT: This study aims to systematically investigate the molecular mechanisms underlying autism spectrum disorder (ASD) by analyzing the proteome and phosphoproteome of a Sh3rf3-deficient mouse model. SH3RF3 (SH3 domain-containing RING finger protein 3) is implicated in synaptic regulation pathways, yet its role in ASD remains poorly understood. Through integrated quantitative proteomics and phosphoproteomics, we seek to:Identify dysregulated proteins and phosphorylation events in Sh3rf3 knockout mice.Uncover signaling pathways and post-translational modifications (PTMs) associated with ASD pathophysiology.Provide a resource for understanding synaptic protein networks regulated by SH3RF3.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain, Cns Neuron (sensu Vertebrata)

DISEASE(S): Autism Spectrum Disorder

SUBMITTER: Yuting Yuan  

LAB HEAD: Zhiheng Xu

PROVIDER: PXD061722 | Pride | 2026-03-23

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
6PLEX_MS_1.raw Raw
6PLEX_MS_10.raw Raw
6PLEX_MS_11.raw Raw
6PLEX_MS_12.raw Raw
6PLEX_MS_13.raw Raw
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Publications

Sh3rf3 Deficiency drives autism-like behaviors via presynaptic dysfunction in mice.

Yuan Yuting Y   Li Yang Y   Yang Fuqiang F   Jiang Yisheng Y   Ding Yuanyuan Y   Xiao Ying Y   Zhu Xili X   Shu Xingmei X   Huang Xiahe X   Wang Yingchun Y   Zhang Shuli S   Sun Jianyuan J   Xu Zhiheng Z  

Molecular psychiatry 20251125


Autism spectrum disorder (ASD) is a prevalent and complex neurodevelopmental disorder with a strong genetic basis. Although SH3RF3 has been identified as an ASD candidate gene, its biological function and pathophysiological mechanisms remain elusive. Here, we reveal that SH3RF3 functions as an essential scaffold protein that facilitates presynaptic vesicle docking. Mechanistically, it orchestrates the formation of a molecular complex between the kinase BRSK1/SAD-B and the ASD-associated active z  ...[more]

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