SURF

Neha Chandra

Investigating the Role of TRIM21 Autoubiquitination in IRF7 Down-Regulation

The innate immune response is the cells first line of defense against viral infection. One of its functions is the production of cytokines, such as interferons (IFN), which are needed to recruit immune cells to the site of infection. In order to create an efficient immune response, IFN production is controlled by highly regulated signal transduction pathways. The E3 ubiqutin ligase protein, TRIM21, has been shown to down-regulate IFN production pathways by targeting the IFN regulatory factor, IRF7, for degradation. However, the factors and mechanism leading to the affinity of TRIM21 for IRF7 upon viral infection are not well understood. I will investigate the importance of TRIM21 autoubiquitination, a protein modification, in promoting TRIM21 activity and interaction with IRF7. Understanding how TRIM21 is activated to regulate interferon production is beneficial in understanding the innate immune response pathway.

Message to Sponsor

This SURF award gives me the opportunity to synthesize what I have learned at Berkeley as an undergraduate into my own honors thesis. Having worked in Professor Winotos lab for two years, I am thrilled to be given the chance to pursue an independent project in order to challenge and expand my knowledge. Even though I plan to pursue a career in medicine, I believe the resources and skills gained from this experience will help shape my academic perspective for the future.
  • Major: Molecular and Cell Biology, Public Policy (minor)
  • Sponsor: Thye Fund
  • Mentor: Astar Winoto, Molecular and Cell Biology