IndraLab

Statements


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"As expected, USP13 overexpression inhibited autophagy and survival of PC12 cells under OGD/R conditions, and Spautin‐1 treatment counteracted these effects."

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"ROR1, after binding to Wnt ligands, triggers non-canonical signaling cascades that increase the level of calcium or decrease the level of cGMP within the cell, and these changes are closely associated with COPD onset and progression.51 SEC14L4 is known to be differentially expressed in COPD.52 USP13, which inhibits autophagy, may be involved in COPD pathogenesis.53,54Among the 11 feature genes, RS1 has not previously been linked to COPD, and our study justifies further exploration of this potential link."

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"Taken together, overexpression of METTL3 significantly recovered the formation of autophagosome and inhibition of autophagy flux caused by depletion of USP13 (Fig. 7a-f)."

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"Spautin-1 inhibits deubiquitinating enzymes USP10 and USP13 and promotes degradation of the BECN1-PI3K autophagy initiation complex, which is required for canonical autophagy induction [30]."

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"Interestingly, Spautin-1-mediated specific and potent inhibition of deubiquitinating activity of USP10 and USP13 was shown to promote proteasomal degradation of PIK3C3 and thereby inhibit autophagy [179]."

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"Because the reductions in the levels of USP10 and USP13 in H4-LC3-GFP cells treated with spautin-1 appeared later than the reductions in the levels of Vps34 complexes and autophagy (XREF_FIG), the reduced levels of USP10 and USP13 are unlikely to be the primary reason for the ability of spautin-1 to reduce the levels of PtdIns3P and inhibit autophagy."

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"The function of USP10 and USP13 is reversed by a chemical compound, spautin-1, which inhibits autophagy by promoting Beclin-1 degradation."