BYU

Abstract by Robert Fender

Personal Infomation


Presenter's Name

Robert Fender

Degree Level

Undergraduate

Co-Authors

Joshua Andersen
Katie Pennington
Katherine McCormack
Eranga Roshan Balasooriya Loku Balasooriya
Colin Muir

Abstract Infomation


Department

Chemistry and Biochemistry

Faculty Advisor

Joshua Andersen

Title

14-3-3zeta Mediation of PTOV1 in Oncogenic Pathways

Abstract

The oncogenic protein Prostate Tumor Overexpressed-1 (PTOV1) is involved in multiple cancer promoting pathways. Our preliminary data suggests that PTOV1 function may be modified through the binding of the regulatory protein 14-3-3zeta. Mechanistically, we have discovered that the mutation of serines S36 or S53 in PTOV1 disrupts binding of 14-3-3zeta. Furthermore, colocalization experiments reveal that loss of 14-3-3zeta binding to PTOV1 through mutation results in nuclear accumulation of PTOV1. Therefore, we propose a model where upstream kinase signaling phosphorylates PTOV1 at S36 and S53, enabling 14-3-3zeta binding. This interaction subsequently prevents PTOV1 translocation to the nucleus thereby preventing its actions as an oncogenic transcription factor. Understanding the mechanism of this oncogenic factor is key to the development of potential cancer therapies that target this pathway.