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. 2009 Apr 17;284(16):10639–10649. doi: 10.1074/jbc.M806508200

FIGURE 1.

FIGURE 1.

Aberrant CaMKII subcellular distribution and GluR1 surface expression in APP transgenic mice. A, diagram showing the procedure of subcellular fractionation of proteins. S, the cytosolic fraction; P1, Triton-soluble fraction in the crude synaptosome fraction, which mainly includes cytosolic proteins in synapses; P2, Triton-insoluble fraction in the crude synaptosome fraction, which mainly includes membrane-associated proteins in synapses. B, Western blots showing the expression of CaMKII (α subunit, β subunit, and autophosphorylated), actin, PSD-95, GluR1, and NR1 in different subcellular fractions in the frontal cortex from wild-type versus APP mice. C, cumulative data (mean ± S.E.) showing the percentage change of CaMKII (α subunit, β subunits, and autophosphorylated) in different fractions from APP mice, compared with wild-type mice. *, p < 0.01, ANOVA. D and E, Western blots and quantifications showing the expression of CaMKII α subunit in Triton-insoluble synaptosome (P2) fraction from different ages (3, 6, 12 months old) of APP mice compared with age-matched wild-type mice. F and G, Western blots and quantifications showing the expression of Ser-831-phosphorylated GluR1, surface and total GluR1, Ser-880-phosphorylated GluR2, total GluR2, and surface and total NR1 levels in the frontal cortex of APP mice compared with wild-type mice. *, p < 0.01, ANOVA.