As a molecular geneticist, I focus on diverse physiologies including growth, development and aging that are controlled by signal transduction networks. Recently, my research has revealed that Sestrin, a stress-inducible protein, is a feedback inhibitor of TOR signaling, and that loss of Sestrin can cause various chronic TOR-associated pathologies, such as fat accumulation, mitochondrial dysfunction, cardiac arrhythmia and muscle degeneration. These phenotypes are quite similar to those associated with obesity, aging and lack of exercise, which are currently some of the major public health issues facing our society. I expect that further research on mammalian Sestrin-family proteins may provide a novel way to attenuate aging and prevent or treat age-associated diseases in humans. Thus, as an independent researcher, I am planning to continue working on the molecular mechanism of the age-associated obesity-prompted diseases and the protective role of Sestrins against those pathological progressions.
My recent scientific discoveries include: (i) Important role of Sestrin2 and 3 in regulating metabolic homeostasis during obesity (Cell Metabolism, 2012, in press); (ii) Suppression of age-associated pathologies by Drosophila Sestrin (Science, 2010, 327:1213 - cover story); (iii) Novel roles for AMP-activated protein kinase in controlling cell shape and mitotic cell division (Nature, 2007, 447:1017); (iv) Mediation of obesity-promoted liver carcinogenesis by inflammatory cytokines TNF and IL-6 (Cell, 2010, 140:197); (v) Conservation of a bacterial stringent response protein in animal species (Nat. Struct. Mol. Biol., 2010, 17:1188). In future, we are planning to continue focusing on the molecular mechanism of the age-associated obesity-prompted diseases and the protective role of Sestrins and autophagy against the metabolic derangements.
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