AI Article Synopsis
- RAD51 recombinase is crucial for repairing DNA double-strand breaks, and BRCA2 and PALB2 help deliver RAD51 to damaged sites for this process.
- PALB2 enhances RAD51’s ability to form the D loop during DNA repair and interacts with RAD51 and RAD51AP1 to boost this process.
- The study highlights PALB2's complex role in chromosomal damage repair, which is significant for understanding cancer and Fanconi anemia caused by PALB2 mutations.
Article Abstract
Homologous recombination mediated by RAD51 recombinase helps eliminate chromosomal lesions, such as DNA double-strand breaks induced by radiation or arising from injured DNA replication forks. The tumor suppressors BRCA2 and PALB2 act together to deliver RAD51 to chromosomal lesions to initiate repair. Here we document a new function of PALB2: to enhance RAD51's ability to form the D loop. We show that PALB2 binds DNA and physically interacts with RAD51. Notably, although PALB2 alone stimulates D-loop formation, it has a cooperative effect with RAD51AP1, an enhancer of RAD51. This stimulation stems from the ability of PALB2 to function with RAD51 and RAD51AP1 to assemble the synaptic complex. Our results demonstrate the multifaceted role of PALB2 in chromosome damage repair. Because PALB2 mutations can cause cancer or Fanconi anemia, our findings shed light on the mechanism of tumor suppression in humans.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950913 | PMC |
| http://dx.doi.org/10.1038/nsmb.1916 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!