Ph.D., 2008, University of California, Berkeley
I am currently a postdoctoral fellow studying nucleotide excision repair (NER) proteins and their contribution to disease. Specific defects in NER proteins lead to Cockayne Syndrome (CS), a devastating human disease in which the average lifespan is 12.5 years. CS is characterized by loss of fat, neuronal degeneration, and other symptoms normally associated with aging. The mechanism by which a defect in a DNA repair pathway leads to such a severe phenotype is poorly understood. The NER progeroid mouse model recapitulates some aspects of human CS but with a two week lifespan. Key questions we ask include: What is the primary affected tissue in the NER progeroid mouse and in CS? We hypothesize that non-replicating cells, including neurons, will be particularly sensitive to loss of NER. Second, can we rescue the phenotype of the NER progeroid mouse? We aim to learn more about the basis of CS and hope this knowledge can be used in the development of proper treatments for CS patients.
Vose, SC, Fujioka, K, Gulevich, AG, Lin, AY, Holland, NT, Casida, JE. Cellular function of neuropathy target esterase in lysophosphatidylcholine action. Toxicol Appl Pharm (2008), 232, 376- 383.
Casida JE, Nomura DK, Vose SC. Organophosphate-sensitive lipases modulate brain lysophospholipids, ether lipids and endocannabinoids. Chem Biol Interact (2008), 175, 355- 364.
Vose SC, Holland NT, Eskenazi B, Casida JE. Lysophosphatidylcholine hydrolases of human erythrocytes, lymphocytes and brain: sensitive targets of conserved specificity for organophosphorus delayed neurotoxicants. Toxicol Appl Pharm (2007), 224, 98- 104.
Quistad BG, Fisher KJ, Owen SC, Klintenberg R, Casida JE. Platelet-activating factor acetylhydrolase: selective inhibition by potent n-alkyl methylphosphonofluoridates. Toxicol Appl Pharm (2005) 205, 149-156.