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. 2008 May 8;27(11):1549–1562. doi: 10.1038/emboj.2008.86

Figure 3.

Figure 3

L1/Nrp1 mediates Sema3A-induced erk phosphorylation. (A) Stimulation by Sema3A of fresh cortical tissue induces erk1/2 phosphorylation, which is reproduced in L1/Nrp1- but not Nrp1-expressing HEK cells. (B) Introduction of dominant-negative FAKΔkin abrogates Sema3A-induced erk1/2 phosphorylation in L1/Nrp1-expressing cells. (C) Sema3A-induced erk phosphorylation is lost in cells expressing Nrp1 and L1−1146 mutant lacking FAK recruitment. (D) Sema3A still triggers erk phosphorylation in cells overexpressing constitutively active FAK (FAKΔFERM) even though this construct blocks the recruitment of endogenous FAK. (E) The blots show bands at 125 kDa (endogenous FAK, FAKWT, FAKΔkin) and at 70 kDa (FAKΔFERM). (F) Sema3A triggers erk phosphorylation in cells expressing L1WT/FAKWT and L1WT/FAKΔFERM but not L1−1146/FAKΔFERM. (G) Introduction of dominant-negative Plex-GPI does not abrogate Sema3A-induced erk1/2 phosphorylation in L1/Nrp1-expressing cells.