Publications by authors named "Aida Badamchi Shabestari"
Article Synopsis
- - The process of DNA double-strand break repair through homologous recombination requires end resection to create a single-stranded DNA template, involving the RAD51 recombinase and other proteins, with BRCA1-BARD1 being crucial for this step.
- - DNA end resection is performed by three key nucleases: EXO1, DNA2 (in partnership with BLM or WRN helicases), working together to resect the DNA ends, while BRCA1-BARD1’s role in regulating this process is critically examined.
- - Research shows that BRCA1-BARD1 directly interacts with EXO1, BLM, and WRN, enhancing their activity, and certain BARD1 mutations impairing DNA
Environmental agents like ionizing radiation (IR) and chemotherapeutic drugs can cause severe damage to the DNA, often in the form of double-strand breaks (DSBs). Remaining unrepaired, DSBs can lead to chromosomal rearrangements, and cell death. One major error-free pathway to repair DSBs is homologous recombination repair (HRR).
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- The BRCA2 tumor suppressor is essential for repairing DNA double-strand breaks through a process called homologous recombination, specifically involving RAD51 protein.
- Research shows that the C-terminal Recombinase Binding (CTRB) region of BRCA2, found in its exon 27, has DNA-binding capabilities that enhance RAD51's ability to facilitate DNA strand exchange.
- The study highlights the importance of CTRB in protecting DNA replication forks during repair processes, suggesting that loss of this function can lead to serious developmental issues, such as embryonic lethality.