RIN1 binds specifically to activated RAS, a common oncoprotein. But RIN1 overexpression inhibits transformation of fibroblast and epithelial cells. This could result from a competitive block of other RAS effector pathways or activation of anti-tumor pathways, or both. We are investigating the specific role of RIN1 as a suppressor of breast tumor initiation and progression. We are also examining the role of RIN1 in leukemias and lymphomas, which often involve increased ABL activity.

RIN1 is expressed at highest levels in mature forebrain neurons. Disruption of the RIN1 gene results in elevated long term potentiation and enhanced aversive memories in mutant mice. We are investigating the function of RIN1 as a negative modulator of neuronal plasticity and memory.

Recent studies suggest that RIN2 and RIN3, two genes closely related to RIN1, have related but distinct signaling functions.

John Colicelli is a cell biologist and biochemist. He joined the Department of Biological Chemistry in the UCLA School of Medicine in 1990. He became a full professor in 2003. Dr. Colicelli earned his B.A. in Chemistry at Rutgers University and his M.S. and Ph.D. in Biochemistry from Columbia University in New York. He was a postdoctoral fellow at Cold Spring Harbor Laboratory. Dr. Colicelli's research is focused on molecular signal transduction in cancer biology and neuronal plasticity. He teaches cell biology at the graduate and undergraduate levels. Dr. Colicelli serves as a Departmental Vice Chair and as a member of the School of Medicine Faculty Executive Committee.