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. Author manuscript; available in PMC: 2012 Mar 23.
Published in final edited form as: Nat Cell Biol. 2011 Apr 10;13(5):550–558. doi: 10.1038/ncb2225

Figure 7. Targeting of the NTRK1 kinase domain to ER exit sites is sufficient to activate NTRK1-mediated downstream signaling.

Figure 7

(a–c) Swept field confocal optics were used to image HeLa cells that had been transiently transfected with mCherry:Sec16B and GFP fusions to either the amino terminus of TFG referred to as GFP:TFG(N) (n=18), the transmembrane and kinase domains of NTRK1 referred to as GFP:NTRK(C) (n=15), or a TFG(N)-NTRK1(C) fusion (n=28), which is equivalent to the oncogene characterized previously (21). Representative color overlays of mCherry:Sec16B (red) and GFP fusions (green) are shown. Scale bar, 10 μm. (d) Bar graph showing the percent co-localization between the GFP fusions described above and mCherry:Sec16B (error bars represent means +/− SEM for each condition; n=15 different cells for each condition and at least 800 unique ER exit sites were examined). (e) Extracts from hTERT-RPE1 cells stably transfected with GFP alone (Control) or various GFP fusions to the NTRK1 transmembrane and kinase domains (as indicated) were separated by SDS-PAGE and blotted using a phospho-specific ERK1-ERK2 antibody (top) and a pan-ERK1-ERK2 antibody (bottom).