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Jonathan Lin, M.d., Ph.d.

Associate Professor
Pathology
UC San Diego
United States of America

Biography

Jonathan Lin received his B.A. in biochemistry from Harvard University and his M.D. and Ph.D. degrees both from Columbia University, where he studied mammalian spinal cord development with Dr. Thomas M. Jessell.  Dr. Lin completed residency training in Anatomic Pathology at Brigham and Women’s Hospital and fellowship training in Ocular Pathology at UCSF, where he also worked with Dr. Peter Walter, to study the molecular mechanism of the mammalian unfolded protein response (UPR).  In addition, Dr. Lin has worked with Dr. Matthew LaVail at UCSF and demonstrated that UPR genes are activated in animal models of retinitis pigmentosa where a heritable mutation in rhodopsin leads to its misfolding and ultimately causes photoreceptor cell death and blindness.  Before coming to UCSD in 2008, Dr. Lin was an Instructor at UCSF in the departments of Pathology and Ophthalmology. Dr. Lin brings his research on the unfolded protein response in human diseases and clinical expertise in eye pathology to UCSD and the Department of Pathology.

Research Interest

Protein misfolding occurs in numerous human diseases including cancer, Alzheimer’s Disease, neurodegeneration, diabetes, Cystic Fibrosis, viral infections, and blindness associated with retinitis pigmentosa due to expression of misfolded P23H rhodopsin in the eye.  Human cells respond to protein misfolding by activating a set of intracellular signaling pathways collectively termed the Unfolded Protein Response (UPR). UPR signaling promotes cell survival by reducing misfolded protein levels in the cell.  If protein misfolding persists, UPR signaling switches to promote cell death.  Our group studies the role of the UPR in the pathogenesis of these diseases that arise from protein misfolding.  We characterize which molecules of the UPR are activated at different stages of disease progression.  We develop genetic and chemical ways to artificially control the UPR in mammalian cells.  We test if artificial manipulation of the UPR can prevent these diseases.  We pursue these experiments in tissue culture or in transgenic animal models.

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