BYU

Abstract by William Tenney

Personal Infomation


Presenter's Name

William Tenney

Degree Level

Undergraduate

Co-Authors

Chrissy Egbert
Tsz Yin Chan
Logan Larsen
Kristina Kohler

Abstract Infomation


Department

Chemistry and Biochemistry

Faculty Advisor

Joshua Andersen

Title

C-Terminus Truncation of TNK1 Promote Kinase Activity

Abstract

TNK1 is a poorly understood non-receptor tyrosine kinase that has been connected to potential oncogenic activity. We discovered that TNK1 kinase activity is regulated by its C-terminal ubiquitin association (UBA) domain. When the C-terminus of TNK1 is truncated to remove the UBA domain, TNK1 becomes a hyper-active kinase. We believe that TNK1's  increased kinase activity promotes survival of cancer cells. We have identified patient cancer cases that possess TNK1 mutations that truncate TNK1, deleting its UBA domain. We are studying these clinical mutations for their cancer-transforming property in a model system with BA-F3 cells.