David Julius, PhD

Professor and Chair
+1 415 476-0431

Our group is interested in understanding how sensory systems enable us to perceive our world. In one aspect of our research, we exploit the power of natural products to elucidate molecular mechanisms of touch and pain sensation. For example, we have asked how capsaicin, the main pungent ingredient in "hot" chili peppers, elicits burning pain, and how menthol, the cooling agent in mint leaves, evokes an icy cool sensation. Using these and other agents as pharmacological probes, we have identified ion channels on sensory nerve fibers that are activated by heat, cold, or chemical irritants, providing molecular insight into the process of thermosensation, pain, and itch. With the aid of genetic, electrophysiological, structural, and behavioral methods, we are asking how these ion channels are modulated in response to tumor growth, infection, or other forms of injury that produce inflammation and pain hypersensitivity. These basic scientific studies are helping to lay a foundation for the discovery and development of novel analgesic drugs.


Sensory TRP Channels in Three Dimensions.

Annual review of biochemistry

Diver MM, King JVL, Julius D, Cheng Y

Irritant-evoked activation and calcium modulation of the TRPA1 receptor.


Zhao J, Lin King JV, Paulsen CE, Cheng Y, Julius D

Structural insights into TRPM8 inhibition and desensitization.

Science (New York, N.Y.)

Diver MM, Cheng Y, Julius D

A Cell-Penetrating Scorpion Toxin Enables Mode-Specific Modulation of TRPA1 and Pain.


Lin King JV, Emrick JJ, Kelly MJS, Herzig V, King GF, Medzihradszky KF, Julius D

Membrane mimetic systems in CryoEM: keeping membrane proteins in their native environment.

Current opinion in structural biology

Autzen HE, Julius D, Cheng Y

Structural insight into TRPV5 channel function and modulation.

Proceedings of the National Academy of Sciences of the United States of America

Dang S, van Goor MK, Asarnow D, Wang Y, Julius D, Cheng Y, van der Wijst J

Tissue-specific contributions of Tmem79 to atopic dermatitis and mast cell-mediated histaminergic itch.

Proceedings of the National Academy of Sciences of the United States of America

Emrick JJ, Mathur A, Wei J, Gracheva EO, Gronert K, Rosenblum MD, Julius D