How cell repair proteins spot and fix DNA damage linked to cancer
Official title: Shu complex and RAD52 function in DNA damage recognition and subsequent repair
Funded at Tufts University Medford · NIH-11167754 · Data updated 2026-11-12
Working to understand how the Shu complex and RAD52 proteins fix DNA damage that can lead to cancer, which matters for people with BRCA2-related risks.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Tufts University Medford NIH-funded |
| Lab location | 1 site (Boston, UNITED STATES) |
| Project start | September 1, 2023 |
| Project end | August 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $249,000 |
| NIH project number | 5R00ES033738-05 |
| Project ID | NIH-11167754 on NIH RePORTER |
Who could benefit from this research
✓Could help
This is laboratory research that does not directly enroll patients, but its results would be most relevant to people with hereditary BRCA2 mutations or cancers tied to DNA repair defects.
✕Less likely to help
People without DNA repair–related cancers or hereditary repair gene mutations are unlikely to receive direct benefit from this lab-focused work.
What this research studies
Researchers will use laboratory experiments in yeast and human cells to study how the Shu complex (SWSAP1/SWS1) and RAD52 respond to DNA damage caused by alkylating agents. They will induce lesions with chemicals like MMS and follow markers such as RAD51 foci, replication fork restart, and R-loop processing. Biochemical assays, microscopy, and binding studies will test how these proteins recognize lesions and help restart stalled DNA replication. The work builds on yeast findings to determine whether the human Shu complex works the same way and how RAD52 contributes to repair pathways linked to BRCA2 and genome stability.
Why it matters
Potential benefit: If successful, this could reveal mechanisms to detect or target DNA repair defects in cancers and guide future therapies for people with DNA repair–linked tumors.
How similar studies have gone: Work in yeast and some human cell studies supports roles for these proteins in DNA repair, but the specific mechanisms of the human Shu complex and RAD52 in replication restart are still largely unproven.
Where this research is happening
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Tufts University Medford
Boston, United States Active
Researchers
- Principal investigator: Hengel, Sarah R — Tufts University Medford
- Study coordinator: Hengel, Sarah R
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.