Rate My Professor Douglas Andres

Douglas A. Andres, PhD, is Professor in the Department of Molecular and Cellular Biochemistry at the University of Kentucky College of Medicine, holding the Antonio S. Turco Professorship in Biochemistry. He earned a Ph.D. in Biochemistry from Purdue University in 1990 under the mentorship of Dr. Jack E. Dixon, a B.S. in Chemistry from the University of Wisconsin-Madison in 1985, and completed postdoctoral training at the University of Texas Southwestern Medical Center in Dallas in 1993 with Drs. Michael Brown and Joseph Goldstein. Andres is affiliated with the Saha Cardiovascular Research Center, Markey Cancer Center, and programs in Molecular and Cellular Oncology and Neuroscience. In 2012, he was named a University Research Professor.

His laboratory investigates how cells respond to environmental signals such as growth factors, hormones, and neuronal firing through Ras-related GTP-binding proteins that function as GTP/GDP-regulated molecular switches in signal transduction pathways. A primary focus is the RIT1 oncoprotein, a regulator of pathways controlling cell growth and differentiation. Using whole-exome sequencing, his team identified somatic RIT1 mutations in approximately 2.5% of lung adenocarcinoma cases among oncogene-negative tumors; these mutations are mutually exclusive with known driver mutations and induce cellular transformation. Research also examines Rit subfamily GTPases in neuronal survival, axonal growth, diabetes, heart disease, and cancer development. Key publications include "Oncogenic RIT1 mutations in lung adenocarcinoma" (Oncogene, 2014), "Mutations in RIT1 cause Noonan syndrome" (Clinical Genetics, 2015), "A Rit GTPase-p38 Mitogen-Activated Protein Kinase Survival Pathway Confers Resistance to Cellular Stress" (Molecular and Cellular Biology, 2011), "Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways" (Oncogene, 2000), and "Rit subfamily small GTPases: Regulators in neuronal differentiation and survival" (Cellular Signalling, 2013). Recent studies explore L-type calcium channel regulation, including "Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity" (npj Regenerative Medicine, 2025). These efforts aim to delineate molecular bases of human disease for novel therapeutic approaches in oncology, cardiology, and neurology.