mRNA decay factor AUF1 maintains normal aging, telomere maintenance, and suppression of senescence by activation of telomerase transcription.
mRNA decay factor AUF1 maintains normal aging, telomere maintenance, and suppression of senescence by activation of telomerase transcription.
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DOI：
10.1016/j.molcel.2012.04.019
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发表时间：
2012-07-13
期刊：
影响因子：
16
通讯作者：
Schneider, Robert J.
中科院分区：
文献类型：
--
作者：
Pont, Adam R.;Sadri, Navid;Hsiao, Susan J.;Smith, Susan;Schneider, Robert J.
Inflammation is associated with DNA damage, cellular senescence and aging. Cessation of the inflammatory cytokine response is mediated in part through cytokine mRNA degradation facilitated by RNA binding proteins, including AUF1. We report a major unrecognized function of AUF1 – it activates telomerase expression, suppresses cellular senescence and maintains normal aging. AUF1 deficient mice undergo striking telomere erosion, markedly increased DNA damage responses at telomere ends, pronounced cellular senescence and rapid premature aging that increases with successive generations, which can be rescued in AUF1 knockout mice and their cultured cells by resupplying AUF1 expression. AUF1 binds and strongly activates the transcription promoter for telomerase catalytic subunit Tert. In addition to directing inflammatory cytokine mRNA decay, AUF1 destabilizes cell cycle checkpoint mRNAs, preventing cellular senescence. Thus, a single gene, AUF1, links maintenance of telomere length and normal aging to attenuation of inflammatory cytokine expression and inhibition of cellular senescence.
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影响因子：
11.4
作者：
Herrera, E;Samper, E;Blasco, MA
通讯作者：
Blasco, MA
影响因子：
4.8
作者：
Enokizono, Y;Konishi, Y;Katahira, M
通讯作者：
Katahira, M
DOI：
10.1098/rstb.2010.0291
发表时间：
2011-01-12
期刊：
Philosophical transactions of the Royal Society of London. Series B, Biological sciences
影响因子：
--
作者：
Donate LE;Blasco MA
通讯作者：
Blasco MA
影响因子：
64.8
作者：
Molofsky, Anna V.;Slutsky, Shalom G.;Morrison, Sean J.
通讯作者：
Morrison, Sean J.
DOI：
10.1111/j.1742-4658.2010.07759.x
发表时间：
2010-09
期刊：
The FEBS journal
影响因子：
--
作者：
Brooks TA;Kendrick S;Hurley L
通讯作者：
Hurley L