Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 34, Issue 11, Pages 2062-2074Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00197-14
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Funding
- Cancer Research UK [C6/A11224, C6946/A14492]
- European Research Council
- European Community Seventh Framework Program [HEALTH-F2-2010-259893]
- Wellcome Trust [WT092096]
- Ministerio de Ciencia e Innovacion [SAF2009-10023]
- Ministerio de Economia y Competitividad [BFU2012-39521]
- FEBS Return-to-Europe
- Early Postdoc Mobility fellowship from the Swiss National Science Foundation
- Cancer Research UK [11224] Funding Source: researchfish
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The DNA damage response (DDR) is critical for genome stability and the suppression of a wide variety of human malignancies, including neurodevelopmental disorders, immunodeficiency, and cancer. In addition, the efficacy of many chemotherapeutic strategies is dictated by the status of the DDR. Ubiquitin-specific protease 28 (USP28) was reported to govern the stability of multiple factors that are critical for diverse aspects of the DDR. Here, we examined the effects of USP28 depletion on the DDR in cells and in vivo. We found that USP28 is recruited to double-strand breaks in a manner that requires the tandem BRCT domains of the DDR protein 53BP1. However, we observed only minor DDR defects in USP28-depleted cells, and mice lacking USP28 showed normal longevity, immunological development, and radiation responses. Our results thus indicate that USP28 is not a critical factor in double-strand break metabolism and is unlikely to be an attractive target for therapeutic intervention aimed at chemotherapy sensitization.
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