53BP1-USP28 cooperation is essential for normal p53-promoter element interactions and gene transactivation-associated events yet dispensable for 53BP1-dependent DNA double-strand repair regulation.
analysis of centrinone resistance identified a 53BP1-USP28 module as critical for communicating mitotic challenges to the p53 circuit and TRIM37 as an enforcer of the singularity of centrosome assembly.
The authors identified 53BP1 and USP28 as essential components acting upstream of p53 evoking p21-dependent cell cycle arrest in response not only to centrosome loss but also to other distinct defects causing prolonged mitosis.
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