Faculty Advisor

Heilman, Destin

Center

University of Massachusetts Medical Center

Abstract

BRCA1 was linked to tumor suppression through its interactions with multiple proteins, which included FancJ. When phosphorylated at Ser990, FancJ was used to repair DNA lesion via homologous recombination. Other than phosphorylation, acetylation at K1249 was observed after DNA interstrand crosslinks (ICLs) induction. The cellÂ’s ability to survive ICL due to camptothecin or mitomycin C was not interfered by preventing FancJ acetylation; however, FancJÂ’s function in the G2/M checkpoint maintenance during cellular division was disrupted by both preventing and mimicking FancJ acetylation, allowing cells to undergo mitosis directly after serious DNA damage.

Publisher

Worcester Polytechnic Institute

Date Accepted

April 2012

Major

Biochemistry

Project Type

Major Qualifying Project

Accessibility

Unrestricted

Advisor Department

Chemistry and Biochemistry

Project Center

University of Massachusetts Medical Center

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