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. 2007 Mar 6;5(4):e63. doi: 10.1371/journal.pbio.0050063

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© 2007 Cheung et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) BDNF stimulation resulted in an increase in p-Ser478 TrkB (p-Ser TrkB) levels in cortical neurons. Treatment with Cdk5 selective inhibitor Ros (25 μM) inhibited the BDNF-induced increase in p-Ser478 TrkB, although Ros treatment also resulted in a slight increase in basal p-Ser478 TrkB.

(B) cdk5 ^+/+ and cdk5 ^−/− brain lysates were immunoblotted against TrkB, phospho-TrkB at Ser478, and β-actin as loading control. p-Ser478 TrkB was almost completely absent in cdk5 ^−/− brain, indicating the importance of Cdk5 in the phosphorylation of TrkB at Ser478 in vivo.

(C) Cortical neurons isolated from cdk5 ^+/+ and cdk5 ^−/− brain were treated with BDNF for different periods. Interestingly, while BDNF enhanced TrkB Ser478 phosphorylation in cdk5 ^+/+ cortical neurons, TrkB Ser478 phosphorylation was not detected in cdk5 ^−/− neurons, nor did BDNF stimulation enhance Ser478 phosphorylation, indicating that BDNF-stimulated increase in TrkB Ser478 phosphorylation requires Cdk5 activity.