The enzyme encoded by this gene is a member of the RAD51 protein family which assists in repair of DNA double strand breaks.

In humans, RAD51 is a 339-amino acid protein that plays a major role in homologous recombination of DNA during double strand break repair.

When these DNA lesions are unrepaired, replication errors can occur near to the damaged sites (see translesion synthesis), leading to increased mutations and cancer.

[26][27] In vertebrates, a number of RAD51 paralogs (see Figure) are essential for RAD51 protein recruitment or stabilization at sites of DNA damage.

The recombinase paralog rfs-1 is found in the round worm Caenorhabditis elegans, however it is not essential for homologous recombination.

[30] In mice and humans, the BRCA2 complex primarily mediates orderly assembly of RAD51 on ssDNA, which is an active substrate in homologous pairing and strand invasion.

[31] However, in the presence of a BRCA2 mutation, human RAD52 can mediate RAD51 assembly on ssDNA and substitute for BRCA2 in homologous recombinational DNA repair,[32] though with lower efficiency than BRCA2.

[33] During meiosis, the two recombinases, Rad51 and Dmc1, interact with single-stranded DNA to form specialized filaments that are adapted for facilitating recombination between homologous chromosomes.

In aged and chemotherapy treated females, oocytes and follicles are depleted by apoptosis (programmed cell death) leading to ovarian failure.

[35] The Rad51-induced oocyte resistance to apoptosis is likely due to Rad51’s central role in homologous recombinational repair of DNA damage.

[39] Further study demonstrated that transfecting breast cancer cells with a vector over-expressing miR-155 represses RAD51 expression, resulting in decreased homologous recombination and increased sensitivity to ionizing radiation.

This repression was generally associated with decreased HR and increased sensitivity of the cells to DNA damaging agents.

The breast cancer susceptibility protein BRCA2 and PALB2 controls the function of Rad51 in the pathway for DNA repair by homologous recombination.

[10][52] In addition to the data listed in Table 1, increased RAD51 expression levels have been identified in metastatic canine mammary carcinoma, indicating that genomic instability plays an important role in the carcinogenesis of this tumor type.

[53][54][55][56] Fanconi anemia (FA) is a hereditary condition characterized by cellular hypersensitivity to DNA cross-linking agents.

A dominant negative mutation in the Rad51 gene has been reported to give rise to an FA-like phenotype with features of mental retardation.