Job Description
The goals of this fellowship are to define the mechanisms by which deregulated kinase signaling in the MAPK, Src, and FAK pathways promote thyroid tumorigenesis. Project #1 focuses on our discovery showing FAK accumulates in the nucleolus to promote ribosome biogenesis to drive thyroid growth and survival. The goals of this project are to determine the mechanisms by which FAK promotes ribosome biogenesis and how to target this novel function in vivo. Project #2 focuses on the mechanisms by which transcriptional reprogramming promotes resistance to BRAF inhibition. These projects will use unbiased approaches (proteomics/transcriptomics) and focused in vitro approaches (Westerns, growth/apoptosis assays, microscopy, invasion/migration assays), along with innovative in vivo models.Together, these tools and approaches will lead to a better understanding of kinase signaling in thyroid cancer and develop durable strategies for targeting the most aggressive forms of the disease.
Application instructions
Full description of the position can be found at CU Careers:
Post-Doctoral Fellow - 32568
https://cu.taleo.net/careersection/2/jobdetail.ftl?job=32568&lang=en