Rishi Hoskeri
Pronouns: He/Him/His
Research Mentor(s): Dipankar Ray
Co-Presenter:
Research Mentor School/College/Department: Radiation Oncology / Medicine
Presentation Date: April 20
Presentation Type: Oral5
Session: Session 1 – 10am – 10:50am
Room: Breakout Room 4
Authors: Rishi Hoskeri, Dipankar Ray, Paramita Ray
Presenter: 7
Abstract
In the progression of Barrett’s esophagus to esophageal adenocarcinoma, the protein Grail isoform 1 of RNF 128 is overexpressed, which stabilizes mutant p53. There is also an isoform-specific role of RNF128 in regulating CD3 expression causing T-cell anergy. The increasing isoform-specific expression of RNF128/GRAIL isoform 1 during Barrett’s progression to esophageal adenocarcinoma (EAC) induces CD3 isoform degradation causing T-cell anergy. Patients with EAC and low CD3 expression in T-cells have decreased survival outcomes compared to those with regular CD3 expression in T-cells. CD3 isoforms delta, gamma, zeta, and epsilon are vital receptor proteins on the cell membrane for T-cell activity. Low CD3 expression has been linked to T-cell anergy, which causes weakened immune responses. The mechanism, iNOS-ISGylation is a key factor in the inhibition of ubiquitination (protein degradation process) of GRAIL isoform 1, helping to stabilize this protein as well as mutant p53. ISG15 knockdown can prevent the degradation of CD3 isoforms preventing T-cell anergy, which can potentially increase the survivability outcomes of patients with Barrett’s esophagus or esophageal adenocarcinoma.
Biomedical Sciences, Interdisciplinary, Natural/Life Sciences
