Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Logo for

Science 332 (6032): 923-925

Copyright © 2011 by the American Association for the Advancement of Science

The TASCC of Secretion

Roberto Zoncu1,2,3, and David M. Sabatini1,2,3,4

The oncogene-induced activation of signaling pathways involving the tumor suppressor proteins p53 and retinoblastoma is likely an important mechanism for preventing the proliferation of potential cancer cells (1, 2). This activation causes cells to exit the cell division cycle and enter a senescent state, which is characterized by major changes in chromatin structure that are thought to render senescence irreversible. Despite the absence of proliferation, senescent cells are not as quiescent as first thought, as they signal to their surrounding environment by activating a protein secretion program (3, 4). On page 966 of this issue, Narita et al. (5) show that to enable this secretory state, a senescent cell profoundly reorganizes its endomembrane system.

1 Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.
2 Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.
3 The David H. Koch Institute for Integrative Cancer Research at MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
4 Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.

E-mail: sabatini{at}

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882