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USP28 activates TP53. 38 / 38
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"Multiple studies indicate that P53 is a downstream target protein of USP28, as USP28 can stabilize and activate P53 [ xref , xref , xref , xref – xref ]."
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"Understanding how 53BP1 and USP28 elevate p53 in response to centrosome loss and extended mitotic duration, and determining whether centrosome loss is an independent input into the p53 circuit or triggers p53 elevation because it leads to sequential prolonged mitoses, are important future goals arising from the results described here."
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"Knockout of 53BP1 or USP28 prevents the stabilization of P53 in cells that experience prolonged mitosis, indicating that 53BP1 and USP28 lie upstream of P53 in this signaling axis (Fong et al. 2016; Lambrus et al. 2016; Meitinger et al. 2016)."
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"A genome-wide CRISPR/Cas9 screen of centrinone-treated cells revealed that depletion of TP53BP1, USP28, or TRIM37 inhibits p53 elevation and alleviates proliferation arrest upon centrosome loss [ 41 ][MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Following p53 localization under such conditions, 53BP1 and USP28 can mediate p53 activation and p21-dependent cell cycle arrest [119]."
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"USP28 depletion decreased p53 protein, but not p53 transcript, levels in BJ cells undergoing replicative senescence (Fig. 2E; Supplemental Fig. S3E,F)."
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"53BP1 responds to mitotic stress, which prolongs mitosis, or to DNA damage and triggers the stabilization of p53 by the deubiquitinase USP28 to stop the proliferation of potentially damaged cells."
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"USP28 overexpression increased the levels of multiple senescence markers, including p53, p21 , and GATA4 proteins but not p16, again suggesting that USP28 may be inducing senescence in part through the p53 and GATA4 branches (Fig. 3C–E; Supplemental Fig. S3K,L)."
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"XREF_BIBR Intriguingly, 53BP1 and USP28 mediated p53 dependent cell cycle arrest in response to centrosome loss and prolonged mitosis."
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"Furthermore, knockout of USP28 prevented P53 up-regulation, consistent with the notion that P53 activation in these microcephaly models occurs through MSP signaling."
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"Previous reports showed that 53BP1 and USP28 activate p53, preventing the proliferation of cells that have an increased chance of mitotic errors [ xref ]."
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"Following p53 localization under such conditions , 53BP1 and USP28 can mediate p53 activation and p21-dependent cell cycle arrest [ 119 ] ."
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"53BP1 and USP28 somehow measure mitotic duration and activate p53 upon mitotic exit."
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"Knockout of USP28 did not alter basal levels of p53 or prevent p53 stabilization in response to doxorubicin induced DNA damage (XREF_FIG and Fig."
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"We conclude that USP28 and 53BP1 do not alter p53 regulation by MDM2 or modulate basal p53 stability."
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"Loss of 53BP1, USP28, and TRIM37 all prevented p53 stabilization and G1 arrest following centrosome loss."
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"Previous reports showed that 53BP1 and USP28 activate p53, preventing the proliferation of cells that have an increased chance of mitotic errors [104]."
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"53BP1 and USP28 somehow measure mitotic duration and activate p53 upon mitotic exit."
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"The mechanism proposed was that 53BP1 and USP28 promote p53 protein stability specifically in the context of mitotic stress, but not by DNA damage or by Nutlin-3."
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"USP28 encodes a deubiquitinase enzyme with substantial evidence from previous biochemistry and cell model studies that link it to p53 activity and apoptotic responses.While it was proposed that USP28 was linked to DNA damage apoptotic responses through the ATM-CHK2-p53 pathway, recent evidence however suggests that a distinct pathway involving TP53BP1 and USP28 induces p53 and cell cycle arrest after mitotic delays [30–35]."
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"Finally, although loss of USP28 or 53BP1 prevents activation of p53 in response to centrosome loss, their loss does not prevent p53 stabilization and cell cycle arrest in cells treated with the DNA damaging agent doxorubicin."
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"Meitinger F, Anzola JV, Kaulich M, Richardson A, Stender JD, Benner C, Glass CK, Dowdy SF, Desai A, Shiau AK, et al. 53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration."
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"ATXN3 and USP28 have been shown to activate TP53 signaling (Liu et al., 2016; Wang et al., 2018b), and knockouts of both of these genes positively correlated with TP53 knockout in DepMap data, supporting the hypothesis that these DUBs are positive regulators of TP53."
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"Termed the mitotic surveillance or mitotic stopwatch pathway, the USP28 and 53BP1 proteins activate p53 in response to delayed mitotic progression to control cell fate and promote genomic stability."
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"53BP1 and USP28 mediate p53 dependent cell cycle arrest in response to centrosome loss and prolonged mitosis."
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"Consistently, overexpression of the wild type USP28 but not USP28 CI in normal, unstressed cells caused ectopic nuclear p53 accumulation and cell cycle arrest uniformly across the entire population (100%, XREF_FIG; not shown)."
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"Meitinger F, Anzola JV, Kaulich M, et al. 53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration."
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"The nuclear p53 accumulation caused by overexpression of wild type USP28 was not due to a specific increase in p53 mRNA levels (XREF_FIG), further supporting our observation that USP28 deubiquitinates p53 for protein stabilization."
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"We showed that 53BP1 and USP28 are required to trigger p53 and p21- dependent cell cycle arrest, evoking an irreversible stress response that selects against unfit cells with disturbed mitosis (XREF_FIG)."
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"Our results furthermore explain how USP28 may modulate the p53 dependent cell cycle checkpoint, thereby controlling tumor cell fate decisions as previously described."
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"Previous reports showed that 53BP1 and USP28 activate p53 , preventing the proliferation of cells that have an increased chance of mitotic errors [ 104 ] ."
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"53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration."
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"Termed the mitotic surveillance or mitotic stopwatch pathway, the USP28 and 53BP1 proteins activate p53 in response to delayed mitotic progression to control cell fate and promote genomic stability."
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"Consistent with the notion that deubiquitination of ub-K119-H2A leads to transcriptional activation, we showed that depletion of USP28 inhibits the transcriptional activity of p53, p21 and p16 INK4a ."
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"Loss of 53BP1, USP28, or TRIM37 suppresses p53 elevation and proliferation arrest triggered by centrosome loss."
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"Homozygosity of either Usp28 or 53bp1 loss reduced p53 activation and rescued brain size in both Sas4 and Cep63 microcephaly models (Figure 2)."
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"In fact, 53BP1- and USP28 deficient cells still up-regulated p53 and arrested in response to the DNA damaging agent doxorubicin, indicating that the DDR is at least partially functional in these cells."
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"USP28Delta cells were used as the control because inactivation of USP28 prevents p53 activation and G1 arrest that is observed as a consequence of delayed mitosis following centrosome loss in RPE1 cells13 ."
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