# Dissecting Mechanisms by which p53 Suppresses Transformation and Radiation Carcinogenesis

> **NIH NIH R56** · DUKE UNIVERSITY · 2020 · $468,865

## Abstract

As humans age, p53 mutations can accumulate in normal tissues. p53 functions as a
transcription factor to drive cell-type dependent responses, such as apoptosis and cell cycle
arrest. Recently, non-canonical functions of p53 have been proposed, such as suppression of
repetitive elements including mobile elements. In this proposal, we will dissect mechanisms by
which p53 regulates repetitive elements using in vitro techniques and in vivo mouse models.
These studies will reveal novel functions of p53 that will not only provide insights into how p53
regulates mobile elements, but will also shed light on the impact of mobile element expression
on the phenotypes of cells and organs. Ultimately, this knowledge will not only be useful for
understanding p53 function, but will also provide insight into mechanisms of normal tissue
aging.

## Key facts

- **NIH application ID:** 10231294
- **Project number:** 1R56AG066487-01A1
- **Recipient organization:** DUKE UNIVERSITY
- **Principal Investigator:** David Guy Kirsch
- **Activity code:** R56 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $468,865
- **Award type:** 1
- **Project period:** 2020-09-15 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10231294

## Citation

> US National Institutes of Health, RePORTER application 10231294, Dissecting Mechanisms by which p53 Suppresses Transformation and Radiation Carcinogenesis (1R56AG066487-01A1). Retrieved via AI Analytics 2026-06-11 from https://api.ai-analytics.org/grant/nih/10231294. Licensed CC0.

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