Comprehensive history and explanation of senescent cells
The Scientist - 01-Mar-2020Including the latest on clinical trials of first-generation senolytics
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Professor of Biochemistry and Molecular Biology and Professor of Pediatrics at The Mayo Clinic.
Jan is passionate about basic medical research and its potential to transform human health and treatment of disease. He has a longstanding interest in questions related to cell cycle control and cellular responses to stress. He helped establish the concept that, with aging and development of age-related disease, wasteful transformed cells that cannot divide litter tissues and organs in small numbers and demonstrated that clearance of these so-called “senescent cells” extends both healthspan and lifespan. During his Ph.D. training, Jan pioneered technologies to knock down the expression of endogenous genes in mice, and these techniques have proven to be particularly useful in uncovering the physiological function of mammalian genes essential to cell division or viability.
In applying these technologies to address the
longstanding question as to whether aneuploidy is a cause or a
consequence of cancer, Jan discovered that BubR1 (an essential mitotic
checkpoint protein that ensures faithful chromosome segregation) is
causally implicated in cancer, progeria and aging. Studies originating
from his desire to understand these mechanisms are credited with
providing the first in vivo evidence that p16-positive senescent cells
drive aging and age-related disease, thus establishing cellular
senescence as a promising target for therapeutic intervention. Dr. van
Deursen holds a B.S. in Biology, M.S. in Molecular Biology, and Ph.D. in
Cell Biology from University of Nijmegen.
Visit website: https://www.mayo.edu/research/faculty/van-deursen-jan-ph-d/bio-00027650
See also: Mayo Clinic - Non-profit American academic medical center focused on health care, education, and research
Details last updated 09-Jan-2020
Including the latest on clinical trials of first-generation senolytics
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Cells accumulate damage in their DNA. Eventually become senescent – i.e. they stop dividing – an...