Elva Diaz, Ph.D.
Department of Pharmacology
UC Davis School of Medicine
I have a broad background in biochemistry, molecular and cell biology and genomics in studies of the mammalian nervous system. I was born and raised in San Jose, CA to parents originally from Mexico. My interest in science and math in high school eventually led me to a career in biomedical research. I earned a bachelor’s degree from Harvard University in Biochemical Sciences in 1993. Following a summer internship at Merck & Co at Rahway, NJ, I pursued graduate studies with Suzanne Pfeffer at Stanford University and earned a Ph.D. in Biochemistry in 1999. My graduate studies involved the molecular mechanisms of receptor trafficking in non-neuronal cells. As a postdoctoral scholar I switched fields into developmental neurobiology and worked with Tito Serafini and John Ngai at UC Berkeley and with Marc Tessier-Lavigne at UCSF. In 2003 I became an Assistant Professor in the Department of Pharmacology at UC Davis School of Medicine and in 2010 I was promoted to Associate Professor with tenure. I was promoted to Full Professor in 2018.
My main research interest is to understand molecular mechanisms of brain development, function and disease. My lab employs functional genomics approaches to identify genes upregulated during distinct phases of brain development. In particular, we focus on two main areas: neural proliferation and synapse development and we have identified several candidate genes involved in these processes. Furthermore, we have shown that misregulation of these genes are implicated in diseases such as brain tumors, substance use, and schizophrenia.
Matt L, Kirk LM, Chenaux G, Speca DJ, Puhger KR, Pride MC, Qneibi M, Haham T, Plambeck KE, Stern-Bach Y, Silverman JL, Crawley JN, Hell JW, Díaz E. SynDIG4/Prrt1 Is Required for Excitatory Synapse Development and Plasticity Underlying Cognitive Function. Cell Rep. 2018 Feb 27;22(9):2246-2253.
Chenaux G, Matt L, Hill TC, Kaur I, Liu XB, Kirk LM, Speca DJ, McMahon SA, Zito K, Hell JW, Díaz E. Loss of SynDIG1 Reduces Excitatory Synapse Maturation But Not Formation In Vivo. eNeuro. 2016 Oct 21;3(5).
Kaur I, Yarov-Yarovoy V, Kirk LM, Plambeck KE, Barragan EV, Ontiveros ES, Díaz E. Activity-Dependent Palmitoylation Controls SynDIG1 Stability, Localization, and Function. J Neurosci. 2016 Jul 20;36(29):7562-8.