Task Mechanism of Clustered DNA Double-strand Break Repair in Response to HZE Particles in Human Cells (Completed)
Last Published:  11/23/20 11:55:12 AM (Central)
Short Title: HZE Clustered DSB Repair
Responsible HRP Element: Space Radiation
Collaborating Org(s):
Funding Status: Completed - Task completed and produced a deliverable
Procurement Mechanism(s):
Solicited
Aims:
The specific aims of the proposed research are to test the hypothesis that:
  1. The cellular ability to repair HZE particles induced clustered DNA damage is modulated by radiation quality and cell cycle stages, utilizing our newly established in situ and imaging technology;
  2. Homologous recombination plays a key function in facilitating the repair of double-strand breaks associated with clustered DNA lesions, using key homologous recombination factors deficient cells;
  3. Fanconi Anemia (FA) complex may orchestrate the repair of complex DSBs induced by HZE particles, using a panel of FA pathway deficient human cells; and
  4. DNA end-processing nucleases, such as Werner Syndrome protein (WRN) and Artemis, may facilitate the processing of complex DNA ends generated by HZE particles using human cells that are either deficient in WRN and Artemis or expressing different nuclease mutant forms of WRN and Artemis.
Resources (None Listed)
Mappings