An NCI-designated Comprehensive Cancer Center

The Fueger Lab

The Fueger Lab works at the intersection of science meant to address diabetes and liver disease. We apply an engineer’s eye to the signaling mechanisms that control metabolism in health — and go awry in disease.
We have a special interest in understanding a particular biochemical signaling pathway that sends orders to divide, die, proliferate or differentiate to cells such as insulin-producing beta cells, affecting metabolism in both the pancreas and the liver. Whereas many studies in diabetes, cancer and metabolism seek to block pathways that contribute to disease when messenger proteins are overexpressed, our investigations may lead to treatments that stimulate pathways that are suppressed.
 
If you would like to contact us for more information, please call 626-256-4673.

Principal Investigator

Patrick Fueger, Ph.D.
Associate Professor, Department of Molecular & Cellular Endocrinology
Role: Principal Investigator
Research Focus: Metabolic Phenotyping

Principal Investigator

Patrick Fueger, Ph.D.
Associate Professor, Department of Molecular & Cellular Endocrinology
Role:Principal Investigator
Research Focus: Metabolic Phenotyping

Lab Members

Halesha Basavarajappa, Ph.D.
Postdoctoral Fellow
 
Brandon Bauer
Graduate Student
 
Kimberley El
Graduate Student
 
Angelina Hernandez-Carretero, Ph.D.
Staff Scientist
 
Jose Irimia-Dominguez, Ph.D.
Staff Scientist
 
Alireza Rezaeizadeh, Ph.D.
Postdoctoral Fellow

Fueger Lab Research Highlights

The Fueger Lab aims to identify and characterize molecular regulators of functional beta cell mass in vitro and extrapolate this work to the in vivo setting. Our studies bridge from isolated cells to more complex biological models, focusing on the protein mitogen-inducible gene 6, or Mig6, which is the endogenous feedback inhibitor of EGFR.
 
Previous studies helped define the roles of molecular brakes and accelerators of beta cell proliferation. We have validated that Mig6 blocks replication in beta cells. Of interest, we have discovered that molecular brakes such as Mig6 impair both beta cell survival and function. Thus, Mig6 can be classified as a multiregulator of functional beta cell mass.