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RPRM (Reprimo) triggers SCF <sup>FBXW11</sup> -mediated DNA-PKcs degradation to block non-homologous end joining and radiosensitize tumors

2025-12-16

Abstract excerpt

Targeting DNA damage repair pathways represents a promising strategy in cancer radiotherapy, however, the limited insight into the regulation of the non-homologous end joining (NHEJ) repair pathway in cancer cells severely restricts the development of precise radiosensitization approaches. Here, we identify Reprimo (RPRM), a p53-inducible tumor suppressor, is a potent inhibitor of NHEJ in which RPRM promotes prote...

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Literature Corpus work
8231d62b-3f03-50ff-beac-cafad1fcd6b3
DOI
10.64898/2025.12.14.694167
Open publication

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RPRM (Reprimo) triggers SCF <sup>FBXW11</sup> -mediated DNA-PKcs degradation to block non-homologous end joining and radiosensitize tumorsDOI 10.64898/2025.12.14.694167
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