Rate My Professor Haining Zhu

Haining Zhu is Professor of Pharmacology and Toxicology at the R. Ken Coit College of Pharmacy, The University of Arizona, holding the R. Ken and Donna Coit Endowed Chair in Aging and Neurodegenerative Diseases. He also serves as Professor in the Department of Chemistry and Biochemistry and the BIO5 Institute, and as Co-Director of the Coit Center for Longevity and Neurotherapeutics. Zhu is a member of the University of Arizona Cancer Center, Southwest Environmental Health Sciences Center, Neuroscience Graduate Interdisciplinary Program, and Cancer Biology Graduate Interdisciplinary Program. He earned a Ph.D. in Chemistry from the University of California, Los Angeles in 2000, completed postdoctoral training in proteomics at Los Alamos National Laboratory in 2002, and received a B.S. in Chemistry from the University of Science and Technology of China in 1994.

The Zhu laboratory investigates RNA binding proteins and RNA metabolism, including protein translation and stress granules, under physiological and pathological conditions. Research examines protein phase separation and aggregation in vitro and in vivo and their relevance to human diseases, with a focus on molecular mechanisms of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), as well as cancer. The group employs mass spectrometry, proteomics, functional genomics, protein chemistry, and biophysics to study protein homeostasis, misfolding, aggregation, and turnover. The laboratory pursues therapeutic development targeting molecules identified in these studies. Key publications include "Lysine acetylation regulates the RNA binding, subcellular localization and inclusion formation of FUS" (Human Molecular Genetics, 2020), "Frontotemporal dementia non-sense mutation of progranulin rescued by aminoglycosides" (Human Molecular Genetics, 2020), "The Acetylation of Lysine-376 of G3BP1 Regulates RNA Binding and Stress Granule Dynamics" (Molecular and Cellular Biology, 2019), "ALS mutations of FUS suppress protein translation and disrupt the regulation of nonsense-mediated decay" (Proceedings of the National Academy of Sciences, 2018), "ALS mutant SOD1 interacts with G3BP1 and affects stress granule dynamics" (Acta Neuropathologica, 2016), and "Self-assembled FUS binds active chromatin and regulates gene transcription" (Proceedings of the National Academy of Sciences, 2014).