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DNA repair protein SWI5 homolog (SWI5) is a conserved nuclear protein involved in homologous recombination-mediated repair of double-strand DNA breaks. In mammals and yeast, SWI5 forms a stable heterodimeric complex with SFR1 (mammals) or Mei5/Sae3 (yeasts), which directly interacts with RAD51, the central enzyme in the HR pathway. This interaction stimulates RAD51 filament formation and strand exchange activity. Experimental depletion of SWI5 causes defects in DNA double-strand break repair, increased sensitivity to ionizing radiation and DNA-damaging drugs such as camptothecin and PARP inhibitors, and results in increased chromosomal aberrations. While SWI5 is essential for maintaining genomic stability, no therapeutics currently target this protein directly. Mutations or deficiencies may contribute to cancer predisposition and other disorders of DNA repair, and SWI5 function is critical for cellular DNA repair responses across eukaryotes[1][4][6][3][5].
Not applicable (no current drugs target SWI5 directly, but cells lacking SWI5 are more susceptible to agents that induce DNA strand breaks). Indirect: inhibitors of molecular partners (e.g., PARP) cause heightened genomic instability when SWI5 is deficient.
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