Pietro De Camilli, MD

John Klingenstein Professor of Neuroscience; Director, Yale Program in Cellular Neuroscience, Neurodegeneration and Repair

Research Interests

Animals, Laboratory; Mental Disorders; Nervous System Diseases; Organisms, Genetically Modified

Research Organizations

Cell Biology: De Camilli Lab | Developmental Cell Biology and Genetics | Membrane Traffic

Diabetes Research Center

Fellowship Training

Interdepartmental Neuroscience Program

Kavli Institute for Neuroscience

NIDA Neuroproteomics Center

Program in Cellular Neuroscience, Neurodegeneration and Repair

Signal Transduction

Signal Transduction

Research Summary

The cytoplasm of eukaryotic cells is compartmentalized by intracellular membranes that are interconnected by membrane traffic. We study mechanisms underlying membrane dynamics, with emphasis on membrane transport reactions involved in neurotransmission. Our goal is to advance the understanding of nervous system function in health and disease, neurodegenerative diseases in particular. We also exploit the special properties of synapses to learn about general principles of membrane biology. Within this field, the interplay between bilayer lipids and peripheral membrane proteins is a major focus of our work. These interactions help regulate membrane budding, membrane fission and membrane progression along the secretory and endocytic pathways. A new interest of the lab concerns the role of lipid exchange between bilayers at membrane contact sites that do not result in membrane fusion. In our work we use a wide range of techniques, including biochemistry, structural biology, cell-free systems, optical and electron microscopy, and mouse genetics

Selected Publications

Edit this profile

Contact Info

Pietro De Camilli, MD
Mailing Address
Boyer Center for Molecular Medicine295 Congress Avenue
BCMM 236

New Haven, CT 06510

De Camilli Lab

Research Image 2

EM tomographic reconstruction: plasma membrane (green lines) and clathrin coated endocytic intermediates in an axon terminal from a neuron that lacks both dynamin 1 and dynamin 3 (dynamin 1 and 3 double KO mouse).