3<i>β</i>-Hydroxysteroid-<i>Δ</i>24 Reductase (DHCR24) Protects Pancreatic <i>β</i> Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species

<div>UPR-related signaling pathways were detected after TM treatment by Western blot analysis. (a) Representative Western blots show the expression of c-myc, Bip, p-p38, ATF6, and cleaved ATF6 in MIN6 cells after TM treatment. The levels of these proteins were normalized to actin levels. 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Journal of Diabetes Research

fig3

Figure 3

Figure 3: 3<i>β</i>-Hydroxysteroid-<i>Δ</i>24 Reductase (DHCR24) Protects Pancreatic <i>β</i> Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species 

Figure 3 | 3β-Hydroxysteroid-Δ24 Reductase (DHCR24) Protects Pancreatic β Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species 