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The simplest scenario (Figure 3) consistent with the existing data thus involves SERT/PP2Ac associa-tions that are enriched in plasma membrane domains containing active SERT, whereas less active SERT pools and inactivated (and possibly recycling) SERTs beingrelatively deficient in SERT/PP2Ac complexes.
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We speculate that p38 MAPKmay either augment or stabilize SERT/PP2Ac associations, or,alternatively, p38 MAPK may enhance PP2A activity withinmembrane-resident, transporter-phosphatase complexes.