IndraLab

Statements

USP28 activates TP53. 24 / 24
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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 mediate p53 dependent cell cycle arrest in response to centrosome loss and prolonged mitosis."
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"53BP1 and USP28 somehow measure mitotic duration and activate p53 upon mitotic exit."
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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 [ xref ]."
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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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"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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"Following p53 localization under such conditions, 53BP1 and USP28 can mediate p53 activation and p21-dependent cell cycle arrest [119]."
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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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"Deletion of TP53BP1, USP28, or TRIM37 prevented p53 elevation in response to centrosome loss but did not affect cytokinesis failure induced arrest or p53 elevation after doxorubicin induced DNA damage."
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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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"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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"53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration."
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"53BP1 and USP28 somehow measure mitotic duration and activate p53 upon mitotic exit."
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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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"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, or TRIM37 suppresses p53 elevation and proliferation arrest triggered by centrosome loss."
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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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"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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"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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"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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"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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"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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"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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