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. 2011 Dec 15;22(24):4854–4867. doi: 10.1091/mbc.E11-07-0592

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© 2011 Larimore et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 3: — PI4KIIα content in synaptosomes of AP-3–deficient mocha mice is reduced. (A) Synaptosome fractions from control brains (lanes 1–8) and AP-3–deficient mocha (Ap3d1^mh/mh) brains (lanes 1′–8′) were resolved on SDS–PAGE, and the contents were analyzed by immunoblot with antibodies against synaptic vesicle markers (SV2, synaptophysin), AP-3–dependent synaptic vesicle cargoes (PI4KIIα, VAMP7, ZnT3), and AP-3 σ3 subunit. (B) Quantification of antigen content expressed as a ratio of the heavy synaptosome fraction from control and AP-3–deficient mocha (Ap3d1^mh/mh) brains. Numbers in parentheses represent the number of independent immunoblots performed from three independent fractionations. *p < 0.0001; **p = 0.0157. HS, heavy synaptosomes; LS, light synaptosomes; Mit, mitochondrial-enriched fractions obtained from Percoll gradients; P1 and P2, low- and high-speed pellets, respectively. Fractions were generated as per Nagy and Delgado-Escueta (1984).