Cell
Volume 32, Issue 4, April 1983, Pages 1026-1028
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Perturbation of vesicular traffic with the carboxylic ionophore monensin

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    To verify band identity and to probe for potential precursor-product relationships, MNT-1 cells were treated with small molecule inhibitors of trafficking and processing steps. Detergent-soluble lysates were then analyzed by non-reducing SDS-PAGE and immunoblotted with HMB45 or αPMEL-C. Treatment of MNT-1 cells with monensin, an inhibitor of intra-Golgi transport (53), led to the accumulation of p250 and higher Mr oligomers as well as the concomitant depletion of p160 (Fig. 6, A and B, lane 2). This supports the conclusion that p250 forms during ER exit or in the early Golgi and that p160 forms in the trans-Golgi network or later.

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