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. 2004 Mar 29;101(14):5075–5080. doi: 10.1073/pnas.0401030101

Fig. 3.

Fig. 3.

NTE localizes to the ER and its deletion results in redistribution of Nissl substance in the thalamic neurons. (A and B) Silver staining showing neuronal loss in the thalamus of a Nes-cre:NTEfl/fl mice mouse (3 months) (A) when compared to age-matched NTEfl/fl mouse (C). (E, F, and G) Fluorescent Nissl stain showing vacuolated neurons in Nes-cre:NTEfl/fl mice. (D) Normal distribution of Nissl substance in the cell body of NTEfl/fl mice. (E) Six-week-old Nes-cre:NTEfl/fl mouse at the onset of neuronal pathology showing two normal and one vacuolated neuron. (H) Subcellular fractionation of hippocampal neurons shows the presence of NTE in the ribophorin, ER-containing fraction, and not in the GM130, Golgi-containing fraction. +, positive control, cerebrum lysate; -, negative control, heart lysate; I, interface between gradients; T, top of gradient; B, bottom of gradient. Double immunofluorescence for calnexin (J) and NTE (I) in primary hippocampal neurons shows association of NTE with the ER (K). (Scale bar, 36 μmin A-C;25 μmin B-D; and 13 μmin E-G.)