Supplementary Materials

Supplementary Materials for:

IRE1α prevents hepatic steatosis by processing and promoting the degradation of select microRNAs

Jie-Mei Wang,* Yining Qiu, Zhao Yang, Hyunbae Kim, Qingwen Qian, Qinghua Sun, Chunbin Zhang, Lei Yin, Deyu Fang, Sung Hong Back, Randal J. Kaufman, Ling Yang,* Kezhong Zhang*

*Corresponding author. Email: kzhang{at}med.wayne.edu (K.Z.); jiemei.wang{at}wayne.edu (J.-M.W.); ling-yang{at}uiowa.edu (L.Y.)

This PDF file includes:

  • Fig. S1. Metabolic phenotype of IRE1α-KO and control mice fed NC or an HFD.
  • Fig. S2. Immunofluorescent staining of IRE1α and S-nitrosylation signals in mouse liver tissues.
  • Fig. S3. miRNA profiles in IRE1α-KO and control livers from NC- or HFD-fed mice and in OA-loaded mouse hepatocytes.
  • Fig. S4. Palmitate represses IRE1α activity in processing select miRNAs.
  • Fig. S5. Titration and duration analyses for the effect of XBP1 overexpression on modulating miR-200 and miR-34.
  • Fig. S6. Expression of the genes involved in lipid and glucose metabolism in IRE1α-KO and control mice fed NC or an HFD.
  • Fig. S7. miRNA-binding sequences of miR-200 and miR-34 family members in the 3′UTRs of human PPARα and SIRT1 genes.
  • Fig. S8. Inhibition of miR-34 or miR-200 rescues Pparα and Sirt1 expression and reduces hepatic steatosis caused by IRE1 deficiency and palmitate treatment.
  • Fig. S9. Overexpression of PPARα or SIRT1 reduces hepatic steatosis caused by IRE1 deficiency with palmitate treatment.
  • Table S1. miRNA functional clusters and previously identified targets.
  • References (5170)

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