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Darren J. Baker
Researcher at Mayo Clinic
Publications - 80
Citations - 15949
Darren J. Baker is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Senescence & Aneuploidy. The author has an hindex of 39, co-authored 69 publications receiving 11756 citations.
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Journal ArticleDOI
BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice.
Darren J. Baker,Karthik B. Jeganathan,J. Douglas Cameron,Michael A. Thompson,Subhash C. Juneja,Alena Kopecka,Rajiv Kumar,Robert B. Jenkins,Piet C. de Groen,Patrick C. Roche,Jan M. van Deursen +10 more
TL;DR: It is shown that mutant mice with low levels of the spindle assembly checkpoint protein BubR1 develop progressive aneuploidy along with a variety of progeroid features, including short lifespan, cachectic dwarfism, lordokyphosis, cataracts, loss of subcutaneous fat and impaired wound healing.
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Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline
Tyler J. Bussian,Asef Aziz,Charlton F. Meyer,Barbara L. Swenson,Jan M. van Deursen,Darren J. Baker +5 more
TL;DR: In a mouse model of tau-dependent neurodegenerative disease, the clearance of senescent glial cells prevents the degeneration of cortical and hippocampal neurons and preserves cognitive function, suggesting that targeting senescent cells may provide a therapeutic avenue for the treatment of these pathologies.
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Senescent cells: an emerging target for diseases of ageing.
Bennett G. Childs,Martina Gluscevic,Darren J. Baker,Remi-Martin Laberge,Dan Marquess,Jamie Dananberg,Jan M. van Deursen +6 more
TL;DR: Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.
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Senescence and apoptosis: dueling or complementary cell fates?
TL;DR: The advantages that the senescence program may have over apoptosis as a tumor protective mechanism, as well as non‐neoplastic functions that may have contributed to its evolution are discussed.
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Cellular senescence in ageing: from mechanisms to therapeutic opportunities
TL;DR: The mechanisms and modulators of cellularsenescence establishment and induction of a senescence-associated secretory phenotype are discussed, and the potential of senolytic and senomorphic therapies in ageing and associated diseases is provided.