Figure 6.
Cer activates the UPR in an endocytosis-independent manner. (A) Agarose gel of Xbp1 cDNA amplicons in AML12 treated with Ctrl/CM ± endocytosis inhibitors (amiloride, nocodazole, nystatin, EIPA). (B and C) Effect of clathrin deficiency on ERS transmission. (B) Knockdown efficiency of AP-2α, CHC, or dynamin siRNA (100 nM) in 293T cells examined by western blot. (C) Agarose gel of Xbp1 cDNA amplicons in WT or clathrin knockdown 293T cells treated with 3T3-L1-derived Ctrl/CM. (D–F) Effect of Cav1 KO on ERS transmission. (D) Cav1 KO efficiency in AML12 cells examined by western blot. (E) Agarose gel of Xbp1 cDNA amplicons in WT or Cav1 KO AML12 cells treated with 3T3-L1–derived Ctrl/CM. (F) Quantification of Xbp1s/Xbp1total by RT-qPCR in WT or Cav1 KO AML12 cells treated with 3T3-L1–derived Ctrl/CM (n = 3). Source data are available for this figure: SourceData F6. Refer to the image caption for details.

Cer activates the UPR in an endocytosis-independent manner. (A) Agarose gel of Xbp1 cDNA amplicons in AML12 treated with Ctrl/CM ± endocytosis inhibitors (amiloride, nocodazole, nystatin, EIPA). (B and C) Effect of clathrin deficiency on ERS transmission. (B) Knockdown efficiency of AP-2α, CHC, or dynamin siRNA (100 nM) in 293T cells examined by western blot. (C) Agarose gel of Xbp1 cDNA amplicons in WT or clathrin knockdown 293T cells treated with 3T3-L1-derived Ctrl/CM. (D–F) Effect of Cav1 KO on ERS transmission. (D) Cav1 KO efficiency in AML12 cells examined by western blot. (E) Agarose gel of Xbp1 cDNA amplicons in WT or Cav1 KO AML12 cells treated with 3T3-L1–derived Ctrl/CM. (F) Quantification of Xbp1s/Xbp1total by RT-qPCR in WT or Cav1 KO AML12 cells treated with 3T3-L1–derived Ctrl/CM (n = 3). Source data are available for this figure: SourceData F6.

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