An Inhibitor of Double Strand Break Repair (Non-Homologous End Joining) in Eukaryotic Cells

DNA damaging agents such as ionizing radiation and chemotherapeutics cause double-strand breaks in cellular DNA. These double-strand breaks interfere with the processes of DNA replication and chromosome segregation and thus are lethal if not repaired. An efficient system to repair double-strand breaks in DNA exists in most mammalian cells. Little is known about the molecular mechanisms underlying double-strand break repair, although several proteins have been implicated in the process. Recently, scientists at Johns Hopkins University and Columbia University have identified a protein from the adenovirus which acts as an inhibitor of the mammalian double-strand break repair system. The adenoviral E4 34-kDa protein inhibits the action of the double-strand break repair system on broken chromosomal DNA as well as on exogenous DNA introduced into the cell. This protein is the first identified inhibitor of double-strand break repair in mammalian cells. Description (Set) Proposed Use (Set) This technology provides for the use of the adenoviral E4 34-kDa protein as an inhibitor of double-strand break repair system in mammalian cells. This technology may have applications in the areas of cancer chemotherapy, gene delivery, and immunotherapy.
Patent (Set) 7,022,496

Patents:
US 7,022,496

Inventor(s): Ketner, Gary W.

Type of Offer: Licensing



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