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OTUD5 increases the amount of GPX4. 7 / 7
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"OTU deubiquitinase 5 (OTUD5), a protein that interacts with GPX4, can promote ferroptosis resistance during ischemia/reperfusion injury by stabilizing GPX4 expression; in turn, hypoxia/ischemia-induced OTUD5 autophagy can destabilize GPX4, leading to ferroptosis-dependent kidney injury (96)."
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"OTUD5 increased GPX4 protein levels and decreased GPX4 ubiquitination in a dose‐dependent manner, whereas ectopic expression of OTUD5 did not affect GPX4 (Figure 4E,F; Figure S5E, Supporting Information), indicating that OTUD5 enzyme activity is indispensable for GPX4 protein stabilization."
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"Notably, OTUD5 overexpression, knockdown or knockout did not impact the mRNA levels of GPX4 (Figure S1A–C), indicating that OTUD5 upregulates GPX4 expression independently of transcriptional level in gastric cancer cells.Subsequently, we determined the regulation of OTUD5 on the half‐life of GPX4."
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"Next, we employed CRISPR‐Cas9 genome editing technology to delete OTUD5 in AGS and mouse forestomach cancer (MFC) cells, and found that depletion of OTUD5 significantly suppressed the expression of GPX4 in both of the cells (Figure 5A,B)."
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"Results revealed that overexpression of wild‐type OTUD5 led to elevated GPX4 protein levels, whereas the catalytic mutant C224S‐OTUD5 did not influence GPX4 expression (Figure 2A), indicating that OTUD5 upregulated GPX4 protein levels depending on its DUB activity."
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"Therefore, we explored whether OTUD5 mediates the regulatory effect of THBS1 on GPX4 expression."
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"Conversely, knockdown or knockout of OTUD5 decreased the endogenous GPX4 protein levels in HEK293T, AGS and HGC‐27 cells (Figure 2C–E)."
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