Rad6Rad18mediated

Rad6 and Rad18 are proteins that play crucial roles in DNA damage response and repair mechanisms in eukaryotic cells. Rad6, also known as Rad6A, is a member of the Rad6 family of proteins, which includes Rad6B and Rad6C. Rad18, on the other hand, is a member of the Rad18 family, which includes Rad18A and Rad18B. Both Rad6 and Rad18 are involved in the homologous recombination (HR) pathway, a key process for repairing double-strand breaks (DSBs) in DNA.

Rad6 and Rad18 form a complex that interacts with the MRN complex (Mre11, Rad50, and Nbs1) and the Rad51 recombinase. This interaction is essential for the recruitment of Rad51 to the site of DNA damage, facilitating the formation of a Rad51 filament that catalyzes the strand invasion step of HR. Rad6 and Rad18 also play roles in the regulation of DNA replication and transcription, further emphasizing their importance in maintaining genomic stability.

Mutations in Rad6 and Rad18 have been linked to various genetic disorders, including Fanconi anemia (FA) and Bloom syndrome (BS). FA is characterized by bone marrow failure, chromosomal instability, and an increased risk of cancer, while BS is associated with chromosomal instability, predisposition to cancer, and developmental abnormalities. These disorders highlight the critical role of Rad6 and Rad18 in DNA repair and genomic stability.

In summary, Rad6 and Rad18 are essential proteins in the DNA damage response and repair mechanisms, particularly in the homologous recombination pathway. Their roles in maintaining genomic stability are underscored by their involvement in genetic disorders such as Fanconi anemia and Bloom syndrome. Further research into the functions and regulation of Rad6 and Rad18 is crucial for understanding and potentially treating these disorders.