Autism-related proteins form a complex to maintain the striatal asymmetry in mice.

ABSTRACT: The brain's hemispheres exhibit profound lateralization, yet the underlying mechanisms remain elusive. Using proteomic and phosphoproteomic analyses of the bilateral striatum - a hub for important brain functions and a common node of autism pathophysiology - we identified significant phosphorylation asymmetries. Particularly, the phosphorylation processes in the left striatum appear more prone to disturbance. Notably, SH3RF2, whose single-copy knockout leads to autism spectrum disorder (ASD)-like behaviors in mice, is uniquely expressed in the striatum, forming a complex with CaMKII (an ASD-associated protein) and PPP1CC. Loss of SH3RF2 disturbs the CaMKII/PP1 "switch", resulting in hyperactivity of CaMKII and increased phosphorylation of its substrate GluR1. In Sh3rf2-deficient mice, heig

SUBMITTER: Jiang Y 

PROVIDER: S-EPMC12485048 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature