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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: Mol Cell Neurosci. 2010 Sep 21;46(1):122–135. doi: 10.1016/j.mcn.2010.08.012

Figure 2. The presence of mutant forms of binding partners caused sequestration of WT NIPA1 in GC and WT atlastin-1 in ER.

Figure 2

Triple immunostaining confirming the colocalization in GC complex of both WT forms of proteins (panels A–D) and in ER (panels A–D, calnexin co-staining not shown). We also observed an accumulation of WT NIPA1 in GC in the presence of studied HSP atlastin-1 mutations (panels E–L), and accumulation of WT atlastin-1 in ER together with mutant forms of NIPA1 (panels M–U). Scale bar = 5μm.