BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice

By D. Baker, Karthik B. Jeganathan, J. Cameron, M. Thompson, S. Juneja, Alena Kopecká, R. Kumar, Robert B Jenkins, P. D. de Groen, P. Roche and 1 more. Nature Genetics, 2004

760 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/139d87676d9ad15ef2a239e651743997d323e63b

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Citations in the corpus

The Human Obesity Gene Map: The 2005 Update (2006, background): “cerevisiae) Age-dependent loss of body fat; reduced lifespan (316)”
Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “These mice express extremely low levels of BubR1, a spindle checkpoint gene responsible for proper chromosome segregation during mitosis, and display an early onset of several age-associated disorders including sarcopenia, cataracts, cachexia, lordo kyphosis, cerebral gliosis, and decreased arterial”
Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis (2009, background): “In addition, hypomorphic alleles that express dramatically reduced levels of BUB1 and BUBR1 have also been generate”
Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. (2007, positive): “…tumor predisposition or acceleration occurs in animal models in which other components of the mitotic checkpoint are partially inactivated and the animals exposed to chemical tumor promoters or other oncogenic stimuli (Babu et al., 2003; Baker et al., 2004; Dai et al., 2004; Rao et al., 2005).”
Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “Mice expressing low amounts of the mitotic checkpoint protein BubR1 due to hypomorphic alleles (BubR1) accumulate senescent cells in several tissues early in life [117] and rapidly develop progeroid phenotypes [118].”
GENECODIS: a web-based tool for finding significant concurrent annotations in gene lists (2007, background): “For example, the NEK2 gene is predominantly expressed in spermatocytes and appears to be associated with meiotic chromosomes in these cells [20]; expression of the gene BUB1B in testis decreases with advancing age, and it may play a role in regulating infertility [21].”
Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice (2016, background): “Recent work suggests senescent cell burden can be dramatically increased by chronological aging or in models of progeria (Lecka-Czernik et al., 1997; Baker et al., 2004; Varela et al., 2005), high-fat feeding (Shi et al.”
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders (2011, neutral): “BubR1 H/H mice have a markedly shortened lifespan and exhibit a variety of age-related phenotypes, including infertility, lordokyphosis, sarcopenia, cataracts, fat loss, cardiac arrhythmias, arterial wall stiffening, impaired wound healing and dermal thinnin”
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016, positive): “Western blotting for p16 Ink4a and mouse anti-actin was performed as described 48 .”