He started his career as faculty at the
University of California, San Francisco in 1989. In 1997, Julius's lab cloned and characterized
TRPV1 which is the receptor that detects
capsaicin, the chemical in
chili peppers that makes them "hot". They found that
TRPV1 also detects noxious heat (
thermoception). TRPV1 is part of a large family of structurally related
TRP (transient receptor potential) cation channels. Animals that lack TRPV1 (using genetic knockouts of the protein) lose sensitivity to noxious heat and capsaicin. Julius's lab has also cloned and characterized
TRPM8 (CMR1) and
TRPA1, both members of the
TRP superfamily. They demonstrated that TRPM8 detects
menthol and cooler temperatures and
TRPA1 detects
mustard oil (allyl isothiocyanate). These observations suggested that TRP channels detect a range of temperatures and chemicals. David Julius's lab has also made contributions to the study of
nociception by discovering toxins that modulate these channels, describing unique adaptations of the channels in diverse species and solving the
cryo-EM structures of numerous channels. Julius’ laboratory also made pioneering contributions to the discovery of
purinergic receptors, both the
P2Y class of
G protein-coupled receptors, and the P2X class of ligand-gated ion channels. This included the cloning of
P2Y12, the receptor for
clopidogrel and related
antiplatelet medications that are widely used to reduce the risk of heart disease and stroke. The group also cloned the
5HT3 receptor, a
serotonin-activated ion channel and the target for drugs such as
ondansentron for the treatment of nausea and vomiting. From 2007 to 2020 Julius served as the editor of the peer-reviewed journal the
Annual Review of Physiology. == Awards ==