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. 2012 Mar 15;287(19):15275–15283. doi: 10.1074/jbc.M112.351817

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© 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 5. — α-Actinin-2 selectively enhances CaMKII association with GluN2B-NMDARs. A, CaMKII was immunoprecipitated from extracts of HEK293 cells (input) expressing GluN1, GluN2B, and CaMKIIα (TT305/6AA or T286A/TT305/6AA; AA-CaMKIIα or AAA-CaMKIIα, respectively) with or without HA-α-actinin-2. Input and CaMKII immune complexes were immunoblotted for GluN1, GluN2B, HA, CaMKII, and phospho-Thr286 (P-T286). Levels of co-immunoprecipitated GluN2B were normalized to input and plotted as mean ± S.E. (n = 5). *, p < 0.05 versus GluN1+GluN2B+AACK. ##, p < 0.01 versus GluN1+GluN2B+AACK+HA-A2. #, p < 0.05 versus GluN1+GluN2B+AAACK. B, similar to A, except GluN2B is replaced with GluN2A.