ArticleScientific reports2026
Phosphoproteomic profiling reveals reversal of dysregulated kinase signaling by nitric oxide inhibition in the Shank3 mouse model of autism.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Autism spectrum disorder (ASD) is a wide-ranging neurodevelopmental disorder characterized by behavioral deficits, including difficulties in social communication and interaction, restricted or repetitive behaviors, and limited interests. The SHANK3 gene encodes a scaffolding protein in the postsynaptic density of glutamatergic excitatory synapses and is one of the highest-confidence ASD risk genes. Our previous studies showed abnormally elevated levels of nitric oxide (NO) in Shank3 models of ASD, and inhibition of the neuronal NO synthase (nNOS) reversed ASD-like behavioral and synaptic phenotypes in these models. Protein phosphorylation is involved in all biological processes in the body, but it is still unknown how protein phosphorylation is affected by the NO signaling in ASD. We studied the global proteome and phosphoproteome of the cortical tissue of the Shank3
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