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- Jeremy E. Purvis
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
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- Kyle W. Karhohs
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
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- Caroline Mock
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
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- Eric Batchelor
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
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- Alexander Loewer
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
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- Galit Lahav
- Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
書誌事項
- 公開日
- 2012-06-15
- DOI
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- 10.1126/science.1218351
- 公開者
- American Association for the Advancement of Science (AAAS)
この論文をさがす
説明
<jats:title>Dynamic Responses</jats:title> <jats:p> Expression of the tumor suppressor p53 is activated in response to cell stress. The dynamics of p53 activation can vary, depending on the stressor, resulting in either pulsatile or constant p53 levels; however, the functional consequence of these different dynamics is unclear. <jats:bold> Purvis <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1440" related-article-type="in-this-issue" vol="336" xlink:href="10.1126/science.1218351">1440</jats:related-article> ) developed a method to control p53 dynamics in human cells. Pulsing p53 selectively activated genes involved in cell cycle arrest and DNA repair, allowing recovery from DNA damage. In contrast, sustained p53 promoted induction of terminal genes leading to cellular senescence. Thus, protein dynamics can affect cell fate decisions. </jats:p>
収録刊行物
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- Science
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Science 336 (6087), 1440-1444, 2012-06-15
American Association for the Advancement of Science (AAAS)