Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.

doi:10.1038/ncb1744

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Article

Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.

Nature cell biology - 1 Jul 2008

Baker Darren J, Perez-Terzic Carmen, Jin Fang, Pitel Kevin S, Pitel Kevin, Niederländer Nicolas J, Jeganathan Karthik, Yamada Satsuki, Reyes Santiago, Rowe Lois, Hiddinga H Jay, Eberhardt Norman L, Terzic Andre, van Deursen Jan M

Abstract excerpt

Expression of p16(Ink4a) and p19(Arf) 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 p16(Ink4a) or p19(Arf) die early of tumours. Here, we show that skeletal muscle and fa...

Topics

Adipose Tissue
Aging
Animals
Biomarkers
Cell Cycle Proteins
Cells, Cultured
Cellular Senescence
Cyclin-Dependent Kinase Inhibitor p16
Eye
Fibroblasts
Genotype
Humans
Male
Mice

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice, Inbred C57BL

Mice, Knockout

Muscle, Skeletal

Neoplasms

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Identifiers

PMID: 18516091
DOI: 10.1038/ncb1744
PMCID: PMC2594014

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-18516091-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.