First and Last Name/s of Presenters

Mirjam GrebencFollow

Mentor/s

Dr. Eun Yong Shim, Dr. Sang Lee

Participation Type

Poster

Abstract

The proliferation of cancer strongly depends on flawless cell replication. DNA repair mechanisms are responsible for the cells to replicate without errors. We focused on studying apex2 and its function in the DNA repair pathway of mammalian cells. In BRCA-mutant tumors, apex2 has been identified as a potential synthetic lethal target. Studies in yeast showed that apn2 reduces the frequency of mutations and repairs damage caused by top1. We used CRISPR-Cas9 to knockout apex2 gene in HCT116 and U-2OS and tested genetic interaction between apex2, tdp1, ercc4 and apex1 using siRNA and drug sensitivity. Our results suggest that knockout of apex2 together with knockdown of tdp1 and ercc4 increased drug sensitivity.

College and Major available

Biology

Location

Digital Commons

Start Day/Time

5-5-2021 1:00 PM

End Day/Time

5-5-2021 4:00 PM

Students' Information

Mirjam Grebenc, Molecular and Cellular Biology, Honors, 2021

Please use the Link to Full Text for the correct Recording of this presentation. Technical difficulties are preventing the removal of the Audio recording in the middle of the page.

Comments

Video Recording of Presentation: https://sacredheart-edu.zoom.us/rec/share/-41fJ6bitOtGQQ3pfTn-tK-at9e8U8H20XWvRkJVjHoKxckZugT9hY8hcE7T8SUU.RrQcuzL1f6KnrG4r?startTime=1619644759000

Prize Categories

Best Multidisciplinary Research or Collaboration, Most Scholarly Impact or Potential, Most Creative

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May 5th, 1:00 PM May 5th, 4:00 PM

Role of APEX2 in DNA Repair Mechanisms

Digital Commons

The proliferation of cancer strongly depends on flawless cell replication. DNA repair mechanisms are responsible for the cells to replicate without errors. We focused on studying apex2 and its function in the DNA repair pathway of mammalian cells. In BRCA-mutant tumors, apex2 has been identified as a potential synthetic lethal target. Studies in yeast showed that apn2 reduces the frequency of mutations and repairs damage caused by top1. We used CRISPR-Cas9 to knockout apex2 gene in HCT116 and U-2OS and tested genetic interaction between apex2, tdp1, ercc4 and apex1 using siRNA and drug sensitivity. Our results suggest that knockout of apex2 together with knockdown of tdp1 and ercc4 increased drug sensitivity.

 

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