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. 2004 Oct 25;167(2):365–375. doi: 10.1083/jcb.200404076

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Copyright © 2004, The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 5. — Fyn is required for a laminin-mediated switch in NRG signaling and for integrin activation to increase survival. (A) Survival of newly formed SFK-depleted oligodendrocytes in the presence of the PI3K pathway signaling inhibitor wortmannin (hatched bars), the MAPK pathway signaling inhibitor PD098059 (light gray bars), or DMSO control (black bars). Lm2 switches NRG-mediated survival from PI3K-sensitive to PI3K-insensitive, and Fyn depletion, but not Lyn depletion, abolishes this effect. Error bars represent SD. (B) Oligodendrocytes treated for 30 min with NRG. PhosphoERK is enhanced by Lm2 in control cells, but not in Fyn(−) cells. (C) Survival of newly formed SFK-depleted oligodendrocytes in the presence (light gray bars) or absence (dark gray bars) of integrin-activating manganese. Integrin activation using manganese increased NRG-mediated survival, and this increase was lost in the absence of Fyn, but not of other SFKs. Error bars represent SD.