ArticleProceedings of the National Academy of Sciences of the United States of America2025
CASKIN2 mediates PTPσ-orchestrated transsynaptic mechanisms at excitatory synapses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Estimating protein isoform abundances with [Formula: see text].Proceedings of the National Academy of Sciences of the United States of America · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Presynaptic active zones (AZs) perform essential functions in orchestrating speedy and accurate neurotransmission. Despite extensive studies on their molecular constituents, it remains unclear how transsynaptic signals are organized at AZs. The two members of the CASKIN family of multidomain scaffold proteins, CASKIN1 and CASKIN2, bind to several AZ proteins and LAR receptor protein tyrosine phosphatases (LAR-RPTPs), and thus likely contribute to presynaptic assembly. Analysis using conditional knockout (cKO) mice deficient for CASKIN1 and/or -2 revealed that CASKIN2, but not CASKIN1, is critical for proper synaptic transmission, synaptic strength, and AZ protein arrangement at glutamatergic synapses. CASKIN1/2 deletion recapitulates
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