The Journal of Neuroscience, November 30, 2005, ():
Soluble 
-Amyloid1-40 Induces NMDA-Dependent Degradation of Postsynaptic Density-95 at Glutamatergic Synapses
J. Neurosci. Roselli et al.
25: 11061
Supplemental data
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Supplementary figure 1
Aβ-induced PSD-95 downregulation requires cdk5 activity
Panels in A and B show Western blots of SK-N-MC cell lysates after transfection with wildtype PSD-95. (A) The Aβ-induced decrease in PSD-95 requires cdk5 activity. SK-N-MC cells were treated (1h) with 6-aminopiridine-sulfanilamide (PNU 112455A; 10 然), KN-93 (16 然), or vehicle, before exposure to Aβ (10 mM, 1h). The inhibitor PNU 112455A prevented the ability of Aβ to reduce PSD-95 levels, whereas the CaMKII inhibitor (KN-93) was without effect. (B) The regulation of PSD-95 levels by Aβ occurs independently of GSK-3β or MEK-1/2 activity. In these experiments, cultures were treated (1h) with TDZT (10 然), UO126 (10 然), or vehicle (DMSO) before being treated with Aβ (10 然, 1h). Neither TDZT nor UO126 were able to block Aβ-induced PSD-95 downregulation. Semi-quantitative data are shown as mean + SD.
