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USP48 activates apoptotic process. 10 / 10
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"We also investigated the effects of USP48 on H. pylori induced apoptotic cell death in gastric epithelial cells."
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"After carboplatin (CBP) treatment, the USP48 ablation increases the apoptosis rate, and the cleaved PARP and cleaved caspase 3 expression levels in ES2, 3AO and A2780 cells."
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"Furthermore, inhibition of USP48 expression through shRNA knockdown in AML cell lines significantly reduced cell proliferation, promoted apoptosis, and induced G1 phase arrest."
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"Furthermore, transfection of A20 protein in USP48-depleted cells before H. pylori infection suppressed caspase cleavage and apoptotic cell death (Fig. 4c), indicating that the protective effect on apoptotic cell death is dependent on the expression of A20."
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"Knockdown of USP48 exacerbated apoptosis induction by H. pylori infection, implying that CSN-associated USP48 supports upregulation of A20 and thereby antagonizes apoptosis of gastric epithelial cells[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Mechanistically, we discovered that caspase-3 recognizes a conserved DEQD motif located at amino acids 611–614 of human USP48 and cleaves USP48 during drug-induced apoptosis."
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"USP48 cleavage in drug induced apoptosis of AML."
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"All the data indicated that inhibition of USP48 expression could decrease growth of AML cells by inducing apoptosis and G1 phase arrest."
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"Caspase 3-specific cleavage of ubiquitin-specific peptidase 48 enhances drug-induced apoptosis in AML."
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"During drug induced apoptosis of AML cells, activated caspase-3 cleaves USP48 through recognizing the conservative motif DEQD located at 611-614 sites of human USP48."
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