Abstract by Kristina Kohler

Personal Infomation

Presenter's Name

Kristina Kohler



Degree Level




Abstract Infomation


Chemistry and Biochemistry

Faculty Advisor

Joshua Andersen


Mechanisms of Upstream TNK1 Regulation Affect Cancer Proliferation and Autophagy


TNK1, a cytosolic tyrosine kinase, promotes cancer proliferation and chemoresistance; it is necessary for the functioning of 14-3-3z, a phospho-binding protein which regulates a variety of pro-survival functions. However, TNK1’s specific role and mechanisms of regulation are unknown. Our lab used confocal microscopy and proteomics-based analyses to characterize TNK1’s interactome, its impact on cell motility and autophagic activity, and its upstream regulation by the tyrosine receptor kinase pDGFR. We propose that pDGFR functions as a molecular switch for activating 14-3-3z-TNK1 binding, resulting in increased cell motility and proliferation. Conversely, when pDGFR is not activated, TNK1 is not phosphorylated and cannot bind to 14-3-3z. Our data suggests that a lack of 14-3-3z-TNK1 binding induces autophagy, a putative mechanism for activating chemoresistance. With a greater understanding of its function and regulation, TNK1 could become a viable therapeutic target for slowing tumor growth and overriding chemoresistance.