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. 2022 May 25;16:834780. doi: 10.3389/fnins.2022.834780

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Copyright © 2022 Rechtzigel, Meyerink, Leppert, Johnson, Cain, Ferrandino, May, Roux, Brudvig and Weimer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SNAP25 coimmunoprecipitations demonstrate synaptic SNARE dysfunction in Cln3^Δ7/8, Cln6^nclf, and Cln8^mnd mice. To analyze core SNARE complex formation, P30 mutant brain lysate was immunoprecipitated with anti-SNAP25 antibody and probed for antibodies directed against STX1B, STX1 (recognizes A and B isoforms), and VAMP. (A) Analyses reveal a significant increase in SNAP25-bound STX1B in CLN3, (B) a significant increase in SNAP25-bound STX1B and STX1, and a significant decrease in VAMP2 in Cln6 mutants, (C) an increased binding of SNAP25 and STX1B in CLN8 mutants. Input ~ 3% total protein loaded on IPs. Two-tailed t-test, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3, mean ± SEM.