# Molecular Functions of Recombination in Genome Stability and Tumor Suppression

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2021 · $359,138

## Abstract

Project Summary/Abstract
 The broad objective of this proposal is to understand the molecular mechanism of homologous
recombination in humans, and to understand how the consequences of defects in recombinational DNA repair
result in chromosomal instability and predisposition to cancers. Understanding the functions of key proteins in
homologous recombination, many of which are tumor suppressors, will provide insight into how mutations in
these proteins can predispose individuals to cancer. We plan to elucidate the biochemical roles and examine
the mechanism of BRCA1, BLM, EXO1, PALB2, WRN, and the RAD51 paralogs functions, as well as the
consequences of the interactions between these proteins, to provide insight into their role in recombinational
DNA repair. We plan to reconstitute the initial steps of human recombinational DNA repair, and thereby
understand the biochemical functions of these proteins. In addition, we will use single-molecule imaging to
reveal the molecular mechanisms by which these proteins act.

## Key facts

- **NIH application ID:** 10092116
- **Project number:** 5R01CA208600-05
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Stephen Charles Kowalczykowski
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $359,138
- **Award type:** 5
- **Project period:** 2017-03-15 → 2023-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10092116

## Citation

> US National Institutes of Health, RePORTER application 10092116, Molecular Functions of Recombination in Genome Stability and Tumor Suppression (5R01CA208600-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10092116. Licensed CC0.

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