| 摘要 |
Several peptides that interact with MmRad51 have been identified including, for example <i>Brca2</i> and <i>M96</i>. Additionally, Rad51 self-associates via the N-terminal region. When a single residue was changed from a conserved lysine to an alanine, the alteration proved toxic to cells. Moreover, a <i>rad51</i> allele that lacked the RecA homology region was also deleterious to cells. In view of the above, it is clear that inhibiting Rad51 function or the function of any molecule that associates with MmRad51, or any molecule in the Rad51 or Rad52 pathways, hinders cell proliferation and/or viability. Accordingly, the described class of molecules, that are capable of blocking critical DNA repair pathways represent a new class of therapeutics for inhibiting the growth and maintenance of human cancer cells, as well as other cell proliferation disorders.
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