New Insights into How Cells Repair Damaged DNA During Replication
Official title: Emerging Mechanisms of Replication-coupled DNA Repair
Funded at California Institute of Technology · NIH-11350953 · Data updated 2026-11-12
A scientist-led project at Caltech is exploring how cells fix dangerous DNA damage that happens when DNA is copied, which is important for preventing cancer and aging.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | California Institute of Technology NIH-funded |
| Lab location | 1 site (Pasadena, United States) |
| Project start | August 1, 2023 |
| Project end | June 30, 2028 |
| Funding year | 2026 |
| Award (this year) | $334,588 |
| NIH project number | 5R01GM151410-04 |
| Project ID | NIH-11350953 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals with bone marrow failure syndromes or cancers linked to DNA repair defects where replication-associated damage plays a role.
✕Less likely to help
Patients without conditions related to DNA repair defects may not directly benefit from this basic mechanistic study.
What this research studies
This research investigates how replication-related DNA cross-links are repaired, focusing on a pathway that involves CMG helicase, NEIL3, and homologous recombination. The study builds on prior work using Xenopus egg extracts to understand when an alternative repair pathway is used to avoid dangerous double-strand breaks. By clarifying which types of cross-links are handled by NEIL3, the project aims to map when this repair avoids creating more genome instability. The findings could illuminate why bone marrow failure and cancer predisposition occur in disorders like Fanconi anemia and suggest new angles for therapies. The work combines biochemistry, genetics, and model systems to connect molecular mechanisms to human disease relevance.
Why it matters
Potential benefit: Could lead to new strategies to prevent or treat DNA repair-related diseases and aging by targeting specific repair pathways.
How similar studies have gone: Previous studies show that alternative repair pathways can resolve certain cross-links without creating dangerous DNA breaks, supporting the plausibility of these mechanisms being clinically relevant.
Where this research is happening
-
California Institute of Technology
Pasadena, United States Active
Researchers
- Principal investigator: Semlow, Daniel — California Institute of Technology
- Study coordinator: Semlow, Daniel
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.