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Figure 1. Mice with acute deletion of p62 (p62icKO) are susceptible to hypoxia. Figure 2. Cardiomyocyte p62 deletion impairs Hif-1α and Nrf2 target gene expression under normoxia and hypoxia. Figure 3. Knockdown of p62 reduces Hif-1α stabilization and its transcriptional in cultured H9c2 rat cardiomyoblasts exposed to hypoxia. Figure 4. Loss of p62 decreases and gain of p62 increases Nrf2 protein expression and transcriptional activity in cultured H9c2 cells. Figure 5. Loss of p62 induces Nrf2 ubiquitination. Figure 6. Nrf2 ubiquitination is mediated by Cullin 3 in H9c2 cells lacking p62. Figure 7. Hypoxia upregulates and loss of p62 dampens Nrf2 protein levels. Supplemental Figure 1. p62cKO hearts show mild cardiac contractile dysfunction and reduced Nrf2 signaling.Supplemental Figure 2. Hypoxic stress decreases Nqo1 protein levels in p62icKO mice. Supplemental Figure 3. Time-course of hypoxia in mice. Supplemental Figure 4. Proteasome inhibition causes accumulation of Keap1 protein and loss of p62 does not alter Nrf2 or Keap1 gene expression. Supplemental Figure 5. Loss of p62 decreases Nrf2 nuclear translocation. Supplemental Figure 6. p62 depletion alters macroautophagy in H9c2 cardiomyocytes. Supplemental Figure 7. p62 depletion heightens Nrf2-Keap1 colocalization. Supplemental Figure 8. Loss of p62 accelerates Nrf2 protein degradation. Supplemental Figure 9. p62 depletion heightens oxidative stress and decreases viability of H9c2 cells.