IndraLab

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"However, this event was markedly abolished by ATG5 knockdown, subsequently restoring the cell proliferation in IR incubated OSCC cells.Finally, we found that USP14 mediated apoptosis was autophagy dependent in IR treated OSCC cells."

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"Our recent study exemplifies the feasibility of such an approach : specifically, we showed that blockade of 19S associated DUBs USP14 and UCHL5 with a small-molecule inhibitor (bAP15 and VLX1570) induces apoptosis in MM cells and overcome bortezomib resistance, with a favorable toxicity profile."

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"Together, this confirmed that USP14 knockdown could resist OSCC cell apoptosis induced by b-AP15 treatment, which indicated that USP14 might be involved in b-AP15-induced apoptosis, further demonstrat[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The combination of enzalutamide, a nonsteroidal antiandrogen, with either knockdown or pharmacological inhibition of USP14 promotes arrest of cell cycle progression and induces apoptosis (Xia et al. 2019)."

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"Interestingly, TgT by itself stimulated apoptosis, but only in adult cells."

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"The overexpression of USP14 in USP14 low expression cell lines promoted cell proliferation and migration, whereas USP14 downregulation suppressed tumor cell proliferation, decreased tumor cell colony number, increased apoptosis rate, and decreased cell migration and invasion."

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"In addition, b-AP15, a novel inhibitor of USP14, selectively blocks the deubiquitylating activity of USP14, decreases viability and inhibits proliferation of MM cells, which is associated with growth [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Together, it was suggested that SPAG5‐AS1 stabilized SPAG5 protein through interacting with USP14 in HG‐treated HPCs, and that USP14 and AKT/mTOR formed a positive feedback loop.3.7 SPAG5-AS1 promoted apoptosis and attenuated autophagy in HG-treated HPCs through SPAG5/AKT/mTOR pathway."

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"The PPAR-gamma agonist TgT attenuated MEHP mediated suppression of apoptosis and stimulation of oxidative metabolism by neonatal neutrophils."

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"We previously confirmed that a specific USP14 and UCH37 inhibitor b-AP15 4 inhibited tumor cell growth and induced apoptosis and in vitro (data not shown)."

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"Selective USP14 and UCHL5 inhibitor b-AP15, induced apoptosis in MM cell lines and in primary MM cells via downregulation of cell division cycle 25C (CDC25C), CDC2, and cyclin-B1, as well as the activation of caspases and unfolded protein response pathways (p-IREalpha, p-eIF2alpha, and CHOP)."

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"Additionally, both genetic and pharmacological inhibition of USP14 significantly suppressed cell proliferation in AR responsive breast cancer cells by blocking G 0 / G 1 to S phase transition and inducing apoptosis."

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"Knockdown of USP14 with the lentiviral vector delivery of shRNA in human hepatocarcinoma SMMC7721 cells suppressed cell proliferation, altered the cell cycle and induced cell apoptosis."

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"For example, TgT stimulated apoptosis and inhibited IL-8 production in adult, but not neonatal cells."

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"Similar results were observed in HN6 cells after USP14 knockdown, also demonstrating that USP14 knockdown with specific shRNA was able to significantly reduce the apoptosis induced by b-AP15."