IndraLab

Statements


TP53 activates USP7. 23 / 23
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"Upregulated USP7 further stabilizes MDM2 protein, which further downregulates p53 protein level."

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"24 The absence of p53 increases cell proliferation in vivo and accelerates atherosclerosis.26 Besides, it is proved that p53 deficiency enhances the LPS-induced ALI in vivo.25 Caveolin-1 is identified a novel transduction factor and involved in the progression of pulmonary emphysema by activating ATM-p53-p21 pathway.28 Moreover, in COPD patients, p53/p21 pathway can be activated by up-regulating USP7 to mediate cell premature senescence."

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"Although deletion of p53 did not completely rescue the embryonic lethality of the hausp knockout, embryonic development was extended in both hausp and p53 double knockout embryos."

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"P53 mediated the regulation of USP7 on the radiosensitivity of LSCC cell line."

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"To determine whether there was increased apoptosis due to p53 activation in hausp knockout embryos, a TUNEL (TdT mediated dUTP Nick-End Labeling) assay was performed on wild-type and hausp knockout embryos of both days E6.5 (XREF_FIG) and E7.5 (XREF_FIG)."

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"To explore how did p53 mediate the regulation of USP7 on the radiosensitivity of LSCC cell line, flow cytometric analysis was performed."

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"Hausp knockout was partially rescued by p53 knockout."

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"The results showed that knockout of p53 did not rescue the lethality of the hausp knockout."

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"Owing to the observation of p53 activation in hausp knockout embryos, we attempted to rescue the lethality of hausp knockout mice by generating hausp and p53 double knockout mice."

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"The concurrent loss of TP53 effectively rescued the cytotoxic effect of USP7 knockout, as also observed for PPM1D knockout (XREF_FIG)."

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"Simultaneously, p53 transcriptionally upregulates the DUB enzyme USP7, which counteracts ubiquitylation, thereby stabilizing p53."

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"Furthermore, USP7 knockdown or inhibition with its inhibitor Almac4, developed by Gavory et al., conferred GC cell sensitivity to T-cell cytotoxicity, reduced proliferation, and induced cell cycle arrest by stabilizing p53, which interacts with USP7 [26,107,121]."

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"Interestingly, the level of Mdm4 showed slight increase in hausp knockout MEFs (XREF_FIG, lane 6 versus lane 5), suggesting p53 activation in hausp knockout MEFs was mainly because of downregulation of Mdm2."

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"Loss of TP53 rescues the effects of MDM2, MDM4, PPM1D, and USP7 inhibition."

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"Knockout of Usp7 in mice results in early embryonic lethality that can not be rescued by p53 knockout, suggesting additional roles of Usp7."

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"10, 13, 14 The identification of these substrates indicates that USP7 controls additional vital cellular functions beyond those mediated by p53 stability."

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"The collective results indicate that USP7 deubiquitinates and stabilizes PRMT1 under high glucose conditions.Based on the finding that p53 overexpression induced downregulation of USP7 in A549 and H1299 cells (Fig. 5L) and USP7 expression was significantly increased upon the addition of pifithrin-α when cells were grown under glucose insufficiency (Fig. 5M), we further investigated the involvement of USP7 in modulation of PRMT1 by p53."

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"HAUSP plays pivotal roles in the stability of p53 and MDM2, raising HAUSP as a potential therapeutic target for tuning p53 mediated anti-tumor activity."

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"Once again, the current study demonstrated the essential roles of p53 independent functions of HAUSP, indicated by the inability to rescue the neonatal lethality of hausp FL/FL; nes-cre mice by concomitant deletion of p53."

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"P53 upregulation by USP7-engaging molecular glues."

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"Collectively, these findings suggest that MLF2 suppresses p53 expression by antagonizing USP7‐mediated deubiquitination of p53.We next asked how MLF2 suppresses p53 expression via USP7."

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"Hdm2 is preferentially targeted by USP7 over p53 under normal unstressed conditions; however, USP7 targets p53 in response to DNA damage."

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"Hydroxylation of p53 on Pro359 increased its interaction with USP7 and USP10, leading to decreased p53 ubiquitination and increased p53 protein levels.P53 is also found a target of PHD1."