Fig. 2: Impairment of PERK/ISR signaling under ER stress confers the ER retention of a subset of proteins, including prominent oncogenic RTKs. | Nature Communications

Fig. 2: Impairment of PERK/ISR signaling under ER stress confers the ER retention of a subset of proteins, including prominent oncogenic RTKs.

From: Pharmacological induction of selective endoplasmic reticulum retention as a strategy for cancer therapy

Fig. 2

a Immunoblotting and ponceau-s staining as for c-MET, EGFR, PERK, and p97 as loading control in HepG2 cells treated with Tg, GSK414, and ISRIB alone or in combinations for 16 h (typical result of three independent repetitions). b Immunoblotting for c-MET, PERK, and p97 in WT HepG2 and in three different clones of PERK KO HepG2 cells, treated either with DMSO or Tg alone for 16 h; c Flow cytometry analysis of surface c-MET, EGFR, and HLA-A in WT HepG2 treated with DMSO, Tg, and GSK414 for 16 h (typical result of three independent repetitions). d, e Comparative proteomics of the surface proteins upon treatment with Tg in absence and presence of GSK414. The differently expressed proteins shown by the volcano plot (d). Significantly upregulated proteins upon the Tg/GSK414 treatment are in red, the downregulated proteins are in blue, according to the FDR of 0.05 and a fold change greater than two. The volcano plot is related to Supplementary Data Files 1, 2. e Functional enrichment analysis of the upregulated and downregulated proteins affected by the Tg/GSK414 treatment. The enrichment score is above 1.7 (solid bars) with the Benjamini p value < 0.005 (dashed bars).

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