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. 2011 Apr 26;9(4):e1001051. doi: 10.1371/journal.pbio.1001051

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Lazaridis 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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DHEA binds with high affinity to TrkA and p75^NTR receptors, initiating the following sequence of events: 1) DHEA induces TrkA-mediated Tyr490-phosphorylation of Shc, ERK1/2, and Akt kinases, controlling the expression and function of apoptotic Bcl-2 proteins; and 2) DHEA promotes the interaction of p75^NTR receptors with effector proteins TRAF6, RIP2, and RhoGDI affecting neuronal cell apoptosis. Our findings suggest that the decision between survival and death among DHEA-responsive cells is determined by the balance of its interactions with TrkA and p75^NTR receptors.