Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency
DJ Baker, C Perez-Terzic, F Jin, KS Pitel… - Nature cell …, 2008 - nature.com
Expression of p16Ink4a and p19Arf increases with age in both rodent and human tissues.
However, whether these tumour suppressors are effectors of ageing remains unclear, mainly
because knockout mice lacking p16Ink4a or p19Arf die early of tumours. Here, we show that
skeletal muscle and fat, two tissues that develop early ageing-associated phenotypes in
response to BubR1 insufficiency, have high levels of p16Ink4a and p19Arf. Inactivation of
p16Ink4a in BubR1-insufficient mice attenuates both cellular senescence and premature …
However, whether these tumour suppressors are effectors of ageing remains unclear, mainly
because knockout mice lacking p16Ink4a or p19Arf die early of tumours. Here, we show that
skeletal muscle and fat, two tissues that develop early ageing-associated phenotypes in
response to BubR1 insufficiency, have high levels of p16Ink4a and p19Arf. Inactivation of
p16Ink4a in BubR1-insufficient mice attenuates both cellular senescence and premature …