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Research Expertise and Interest

Structural Biology, reconstitution, membrane biology, autophagy, HIV, x-ray crystallography, cryo-electron microscopy

Research Description

The interplay between proteins and membrane lipids is central to almost every aspect of cell biology. This laboratory is interested in fundamental questions of how the interactions between proteins and membranes determine cell and organelle shape and the evolution of shape over time, how protein-membrane interactions turn on and off the signals that control essential cell processes, and how this information can be used to intervene therapeutically in neurodegenerative disease and viral infection. The lab currently focuses on  (1) basic mechanisms of autophagy, (2) mitophagy and its role in Parkinson's disease, (3) lysosome biogenesis, damage, and repair in cancer and Alzheimer's disease, (4) the function of the C9orf72 complex in amyotrophic lateral sclerosis and frontotemporal degeneration, and (5) hijacking of membrane traffic by HIV. The major approaches used in the lab are cryoelectron microscopy (cryo-EM), cryoelectron tomography (cryo-ET), in vitro reconstitution, and mechanistic cell biology.

In the News

$14 million boost for Parkinson’s disease research

Two new grants totaling nearly $14 million over three years will jump-start research at UC Berkeley into the molecular and genetic causes of Parkinson’s disease, a neurodegenerative disorder that afflicts more than 1 million Americans, yet whose cause remains a mystery.

National Academy, Royal Society elect new UC Berkeley members

Chemist Dean Toste, biochemist James Hurley and astrophysicist Eliot Quataert are the latest University of California, Berkeley, faculty members elected to the prestigious National Academy of Sciences (NAS), a group that has provided policy guidance to the U.S. government since 1863.

Here’s how early humans evaded immunodeficiency viruses

For hundreds of thousands of years, monkeys and apes have been plagued by simian immunodeficiency virus (SIV), which still devastates primate groups in Africa. Luckily, as humans evolved from these early primates, we picked up a mutation that made us immune from SIV — at least until the early 20th century, when the virus evolved to get around our defenses, giving rise to human immunodeficiency virus (HIV) and an AIDS pandemic that today affects an estimated 38 million people worldwide. University of California, Berkeley, researchers have now discovered how that long-ago human mutation interfered with SIV infection, a finding that could provide clues for the development of new therapies to thwart HIV and similar viral infections.

Aiding Cells’ Strategy to Survive

The Bakar Fellows Program supports James Hurley’s research to develop a drug that can help neurons and other cells clear out debris – a process essential for cell survival.

Featured in the Media

Please note: The views and opinions expressed in these articles are those of the authors and do not necessarily reflect the official policy or positions of UC Berkeley.
May 5, 2020

Chemists elected to National Academy of Sciences

Chemical & Engineering News
Linda Wang
Molecular and cell biology and biochemistry professor James Hurley and chemistry professor Dean Toste have been elected to the National Academy of Sciences. According to this reporter: "Election to NAS, which is more than 150 years old, recognizes scientists and engineers for their distinguished and continuing achievements in original research and is considered one of the highest scientific honors bestowed in the US. This year, 23 of the newly elected are members of the American Chemical Society or work in areas related to the chemical sciences." For more on this, see our press release at Berkeley News.
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August 26, 2019

Here's how early humans evaded immunodeficiency viruses

Technology.org
At least until the early 20th century, humans had a mutation that protected us from the simian immunodeficiency virus (SIV) that had plagued monkeys and apes for hundreds of thousands of years, but then the virus evolved to get around the mutation, and that led to the HIV and AIDS pandemic currently suffered by some 38 million people around the world. Now a team of Berkeley researchers has discovered how that protective mutation worked, and they hope it will help scientists develop new treatments to protect against HIV and similar infections. "The main importance for this paper is that it tells us what was one of the last major barriers before the crossover to humans happened," says molecular and cell biology professor James Hurley, the study's lead author. "The current paper is an archeological look at how this happened." This story originated at Berkeley News.
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