RAD (DNA repair) 抑制因子

The RAD protein family in humans plays a crucial role in DNA repair signaling, essential for maintaining genomic integrity and preventing mutations. RAD proteins in yeast were originally identified as radiation-sentitive gene products involved in mitotic/meiotic recombination,and mating-type switching. Key members of this family, such as RAD51, are involved in homologous recombination, a precise method of repairing double-strand breaks in DNA. RAD proteins recognize and respond to DNA damage, recruiting and coordinating with other proteins to facilitate repair. Mutations or dysfunctions in RAD genes can lead to impaired DNA repair, contributing to genomic instability and increasing the risk of cancer development. These proteins also interact with the BRCA1 and BRCA2 genes, further highlighting their importance in hereditary breast and ovarian cancers. Overall, the RAD protein family is integral to the complex and vital process of DNA repair, safeguarding cell health and preventing malignant transformation.

Targeting the RAD protein family or DNA repair pathways for disruption or inhibition has become a strategic approach in cancer therapy. By inhibiting these pathways, particularly in cancer cells that already have compromised DNA repair mechanisms, can induce synthetic lethality, where the accumulation of unrepaired DNA damage leads to cell death. This approach is especially effective in cancers with BRCA1/2 mutations, which are reliant on alternative repair pathways like those mediated by RAD proteins. Additionally, such targeting can sensitize tumors to radiation and chemotherapy, as these cause DNA damage that requires effective repair pathways.