NIH R01 · 2025
Elucidating the molecular mechanism and physiological relevance of TIRR mediated inhibition of p53
53BP1 influences genome stability via two independent mechanisms: (i) a direct role in DNA double-strand break (DSB) repair, (ii) enhancing the activity of p53 as a transcription factor. The role of 53BP1 in DSB repair has been well described with a large body of literature. However, there is very limited understanding of how 53BP1 impacts p53 with contrasting reports on mechanism and function. Perturbing ‘normal’ mitosis caused a p53- dependent cell cycle arrest which was dependent on 53BP1 and its known interactor USP28. The suggested mechanism was that 53BP1/USP28 played a role in the stability and nuclear localization of p53. Another study reported that 53BP1/USP28 accentuated the…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.