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Assistant Professor
(PhD – Vanderbilt University)
Dr. Chrystal Starbird’s Linked in profile

Equity and Inclusion Committee Member: Access and Success

Member, Lineberger Comprehensive Cancer Center
Member, Pathobiology and Translational Science Program

Trained Faculty Mentor endorsed by Office of Graduate Ed UNC Chapel Hill

Research Topics

Receptor Signaling, Protein-Protein Interactions, Structural biology, Crystallography, Cryo-EM

Honors and Awards

  • K99/R00 Career Transition Award under the Maximizing Opportunities for Scientific and Academic Independent Careers (MOSAIC) program, part of the National Institutes of Health, 2021-current
  • Distinguished Service Award in DEI, Yale University, 2022
  • Juneteenth Best Peer to Peer Mentor Postdoctoral Award, Vanderbilt University, 2022
  • Rising Black Scientist Award from Cell Press, 2021
  • Ruth L. Kirschstein Postdoctoral Fellowship from the National Institute of General Medical Sciences, 2019-2021

and many more awards including a Graduate Research Fellowship from the National Science Foundation


Receptor tyrosine kinases are clinically important family of receptors that act as key regulators of a wide range of biological functions. Our lab is broadly interested in the structural and functional principles that guide receptor tyrosine kinase signaling, including understanding how lipids contribute to receptor signaling. Traditionally, when investigating signaling pathways there has been a focus on how interactions between signaling molecules (i.e. ligands) and receptors toggle receptor between activated or inactive states, but it’s becoming increasingly clear that there is much more complexity to receptor tyrosine kinase (RTK) activation. Importantly, improving our understanding of these processes allows us to explore alternative strategies for treatment in diseases where aberrant signaling occurs.

To better understand the structural basis of RTK signaling, my lab is currently focused on studying TAM (Tyro3, Axl and Mer) receptors. TAMs are a mechanistically understudied RTK subfamily whose activation appears to involve not only ligand but also interactions with the membrane lipid, phosphatidylserine. These non growth-factor associated receptors have a vital role in maintaining cellular homeostasis through the clearance of apoptotic cells and control of inflammatory and immune responses and, because of this, dysregulation of TAM receptors is implicated in numerous diseases including autoimmune diseases and cancer. How TAM receptors are activated is an important basic question that my lab aims to address through structural, biochemical, and cellular studies. Additionally, we are interested in investigating the structures of other receptors and transporters that interact with the lipid phosphatidylserine and appear to have overlapping roles with TAM receptors in diseases such as Alzheimer’s disease, to improve our basic understanding of how the lipid microenvironment may impact important cellular processes.


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Chrystal Starbird