The homologous recombination (HR) mechanism is used for high-fidelity DNA repair after double-strand breakage (DSB) and the recovery of collapsed and stalled DNA replication forks. BRCA2 is a classical mediator protein in HR, replacing RAD52 in humans as the principal mediator of RAD51 filament assembly on RPA-coated ssDNA (single stand DNA). The BRCA2 protein is also a principal ovarian and breast cancer susceptibility gene and functions as one of the several mediators that facilitate presynaptic filament formation in human recombination of DNA. RAD51 is an essential gene and its deletion leads to embryonic lethality, which demonstrates the critical role of HR to recover stalled/collapsed replication forks during normal cell proliferation. The purpose of this research project is to study the RAD51 filament formation focused on human BRCA2 and RAD52 to understand what regulates HR and RAD51 filament formation. By studying these interactions, the roles of BRCA2 and RAD52 in regulating HR can be determined and studied for future works in this field. The plasmids containing the GST peptides were generated and sequenced and the protein purification for both RAD52 and BRCA2 was completed. After obtaining the GST-tagged peptides, the protocol for studying the binding of the peptides to RAD51 ssDNA was established. Following optimization of this protocol, interactions between human RAD52 and BRCA2 with RAD51 and the effect on filament formation could be determined.