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. Author manuscript; available in PMC: 2011 May 18.
Published in final edited form as: Dev Cell. 2010 May 18;18(5):750–762. doi: 10.1016/j.devcel.2010.03.009

Figure 7. PTP- and ERK-independent function of SHP2 is conserved in neuroblastoma cells.

Figure 7

(A) Immunoblot of lysates from neuroblastoma cell lines transduced with control shRNA or SHP2-shRNA#3. SHP2 and p-ERK1/2 levels are reduced by shRNA#3 in all cell lines (lanes 2, 4, 6), but only KELLY cells exhibit increased PARP cleavage (lane 2). (B) KELLY cells transduced with SHP2-shRNAs (#1–3) have decreased SHP2 and ERK1/2 levels and increased PARP cleavage (compare lane 1 to lanes 2–4). PARP cleavage caused by shRNA#3 is rescued by co-transduction of wild-type zebrafish zshp2, PTP-impaired (A462T) or PTP-dead (A462T/R466M) zshp2. Exogenous WT zshp2 partially rescues p-ERK1/2 levels (while LS or LS/PTP-dead zshp2 have mild dominant negative effects). (C) shRNA#3 induces cell death in ~ 30% of the infected KELLY cells (TUNEL stain). Co-transduction with zebrafish constructs reduces the cell death caused by shRNA#3. **p <0.001. (D) Model showing phosphatase-dependent and –independent functions of Shp2 during neural crest development. See text for details and Figure S4 for supporting data.