IndraLab

Statements



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"Ectopic expression of C120S-POH1, the enzyme dead mutant with the capacity of maintaining overall proteasomal activity, did not rescue the suppression of cell proliferation caused by endogenous POH1 deletion (XREF_SUPPLEMENTARY)."

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"They subsequently optimized the structure of 8TQ using the FBDD approach to summarize SARs and identified the first potent and specific Rpn11 chemical probe, capzimin (IC  = ∼300 nmol/L), which inhibited the proliferation of bortezomib-resistant cancer cells by stabilizing the proteasome substrates and inducing an unfolded protein response."

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"Recently, a specific inhibitor of PSMD14, capzimin, has been discovered to inhibit PSMD14 and proteasome function, and then suppress the proliferation of tumor cells [ 56 , 57 ], providing a novel ins[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Down-regulation of PSMD14 inhibited the viability, proliferation, and invasiveness of osteosarcoma cell lines."

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"PSMD14 knockdown resulted in G0/G1 arrest, reduced expression of cyclin D1, and attenuated cell proliferation [90], whereas USP21 deubiquitinated and stabilized the transcription factor forkhead box M1 (FOXM1), which is crucial for G2/M transition [91]."

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"POH1 Knockdown Inhibits Cancer Cell Proliferation."

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"The reciprocal effects of knockdown and overexpression of PSMD14 in vitro suggested that PSMD14 enhanced the proliferation ability of HCC cells."