# Characterizing the Regulation of Ferroptosis

> **NIH NIH R01** · STANFORD UNIVERSITY · 2020 · $329,267

## Abstract

Project Abstract
Ferroptosis is an iron-dependent, oxidative cell death pathway implicated in tumor suppression
and pathological cell death. This process is biochemically distinct from apoptosis, classic necrosis
and iron overload-induced cell death. How ferroptosis is regulated at the molecular level is poorly
understood. Guided by preliminary data, this research will test the hypotheses that ferroptosis is
regulated by mechanistic target of rapamycin (mTOR) signaling and neutral lipid synthesis.
Moreover, imaging studies using existing and newly discovered antioxidant inhibitors of
ferroptosis will pinpoint the cellular sites of lethal iron-dependent lipid reactive oxygen species
(ROS) accumulation during ferroptosis and examine how this accumulation is affected by mTOR
signaling and neutral lipid synthesis. These studies will be performed in human cells with the aid
of a novel time-lapse cell death imaging system and techniques drawn from chemical biology,
genetics and biochemistry. This research will advance the understanding of ferroptosis at the
molecular and cellular levels and lay the foundation for future in vivo studies of this poorly
understood cell death process.

## Key facts

- **NIH application ID:** 9995512
- **Project number:** 5R01GM122923-04
- **Recipient organization:** STANFORD UNIVERSITY
- **Principal Investigator:** Scott Dixon
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $329,267
- **Award type:** 5
- **Project period:** 2017-09-05 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9995512

## Citation

> US National Institutes of Health, RePORTER application 9995512, Characterizing the Regulation of Ferroptosis (5R01GM122923-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9995512. Licensed CC0.

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