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. 2005 Dec;16(12):5819–5831. doi: 10.1091/mbc.E05-07-0685

Figure 1.

Figure 1.

Induction of the UPR in J558L and NIH 3T3 cells. J558L cells were treated with 10 mM DTT (A-D) and NIH 3T3 cells were treated with 500 nM thapsigargin (E-H) for the indicated times. (A) Protein synthesis was measured by the metabolic incorporation of [35S]methionine/cysteine into TCA-insoluble material. (B and E) By similar methods, immunoprecipitation protocols were used to assess J558L Ig light chain, GRP94, and Sec61α synthesis rates. (C) Immunoblot analysis of phospho-eIF2α versus eIF2α levels in DTT-treated J558L cells. (D) ATF4 and XBP-1 expression versus β-actin loading control in DTT-treated J558L cells. (F) SDS-PAGE profile of newly synthesized [35S]methionine/cysteine-labeled proteins in thapsigargin-treated NIH 3T3 cells. (G) Northern blot depicting thapsigargin-induced CHOP mRNA expression in NIH 3T3 cells, with ethidium bromide stain of rRNA as a loading control. (H) Immunoprecipitation of [35S]methionine/cysteine-labeled GRP94 after thapsigargin treatment of NIH 3T3 cells.