Brian K. Kennedy, Ph.D., has an international reputation for his work in the basic biology of aging. He became the Buck Institute’s second CEO in July, 2010, coming from the University of Washington in Seattle where he served in the Department of Biochemistry.

Kennedy earned his Ph.D. from the Massachusetts Institute of Technology.  He is well known for work during his graduate studies with Leonard Guarente PhD, which led to the discovery that Sirtuins (SIR2) modulate aging. His current work involves nutrient signaling pathways linked to dietary restriction, particularly the TOR pathway.  He also studies A-type nuclear lamins, which are targets for mutation in Hutchinson-Gilford progeria syndrome.

A native of Louisville, Kentucky, Dr. Kennedy has served on the National Institutes of Health Cellular Mechanisms of Aging and Development study section since 2006, and on the grant review committee for American Federation for Aging Research Grants since 2006. He has published more than 60 manuscripts in prestigious journals including Cell, Nature, Science, and the Proceedings of the National Academy of Sciences. He has been an Associate Editor for the Journal of Gerontology since 2006, and also serves as a consultant for biotech and pharmaceutical companies.

I graduated in September 2011 at the Institute for Biomedical Aging Research in Innsbruck, Austria. In the course of my PhD thesis, which was about aging of human mesenchymal stem cells in the context of the immune system, I became experienced in stem cell biology, biology of aging and cell culture techniques. At the Buck Institute, I will focus on changes in histone modification patterns with stem cell aging, and investigate histone code readers and writers involved in the aging process by both in vitro approaches and mouse models.

Steven joined the Kennedy lab as a graduate student in 2007 after completing his degrees in Biochemistry, Cell and Molecular Biology and Music at the University of Washington. He remained in Seattle to finish his PhD in the lab of Paul Lampe at the Fred Hutchinson Cancer Research Center. He has worked on many different projects, but his current work attempts to elucidate the molecular mechanism behind the development of dilated cardiomyopathy and conduction defects in laminopathies by studying lamin-deficient mice and cells. He is slated to graduate in 2012.

Chen-Yu is a Postdoctoral Fellow in the Kennedy lab. He got his PhD in Physiology at the Barshop Institute, University of Texas Health Science Center at San Antonio. Chen-Yu has studied the genetic variation in the murine lifespan response to dietary restriction. Chen-Yu continues his training in the field of aging research at the Buck Institute. His main focus lies in the molecular mechanisms underlying the aging process in mice.

Mark McCormick is a postdoc in the Kennedy Lab. He completed his PhD in Cynthia Kenyon's lab at UCSF. Mark studies basic mechanisms of aging in the lab, using S. cerevisiae as a model system.

Chris is a Dominican Master's student who joined the lab in August 2010. Previously he received his degree in Biological Sciences and a minor in Chemistry also from Dominican University of California. Here at the Buck, his research mainly focuses on the model organisms of Saccharomyces cerevisiae and Caenorhabditis elegans along with the effects of different compounds and drugs in relation to lifespan.

Marc Ting received his Bachelors of Science in Biology in May of 2011 at Dominican University of California. He joined the Kennedy Lab as an undergraduate in January 2011 as a yeast dissector for the replicative lifespan project. He is currently under the supervision of Dr. Mark McCormick as a laboratory technician working with his recent projects involving the examination of conserved pathways between of S. cerevisiae and C. elegans.

I received my Ph.D in Molecular Genetics from Ohio State University. My graduate project was to study the molecular mechanism of Rb-E2F in early development and late tumorigenesis. Rb-E2F pathway is implantable in cell cycle regulation and cell death commitment. The E2F family is identified as a family of transcription factors, whose target genes are involved in regulation of multiple cellular homeostasis. In Dr. Brian Kennedy’s lab I work on the molecular relevance of mTOR mediated translation and longevity. I have established several genetic mouse models to test the hypothesis derived from yeast and worms, whether alternation of translation can extend mouse health lifespan. From transcription to translation, the most important thing is to thoroughly understand how gene expression is regulated and how this regulation is relevant to longevity.