IndraLab

Statements

USP4 activates TP53. 6 / 6
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"However, in response to cisplatin treatment, USP4 deficiency significantly augmented melanoma cells apoptosis by activating p53 signalling."
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"However, in response to cisplatin induced stress, the knockdown of USP4 could markedly increase the apoptotic rate of melanoma cells, and USP4 deficiency sensitized melanoma cell to cisplatin induced apoptosis by activating p53 pathway."
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"In addition to these newly identified nuclear functions, both USP4 and USP15 are well known to function in the cytosol, i.e. USP4 modulates the Wnt and beta-catenin, NF-kappaB, p53 and TGF-beta signaling pathways while USP15 performs functions in the TGF-beta receptor and NF-kappaB signaling pathways."
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"In contrast, silencing USP4 by shRNA remarkably increased the p53 activity in response to DNA damage or not (XREF_FIG)."
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"Notably, studies have also indicated functions for USP4 in regulating growth factor signalling by the Toll-like receptor/IL1 pathway [88] , TGFb receptor type I [89, 90] , TNFa receptor [91] , growth factoractivated kinase regulation [92] and Wnt signalling [93] , making USP4 a prime target for further evaluation as an oncology drug target with strong potential in DDR contexts.Depletion of USP5 has been reported to cause accumulation of nuclear p53 and increase p53 transcriptional activity."
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"Similarly, knockdown of USP4 significantly decreases cell viability in a p53 dependent manner after treating GMB cells with temozolomide."
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