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Science 337 (6097): 925-926

Copyright © 2012 by the American Association for the Advancement of Science

Glycosylation to Adapt to Stress

Katherine R. Mattaini1, and Matthew G. Vander Heiden1,2

The metabolism of cancer cells differs from that of nontransformed cells (1), yet the mechanism for regulating metabolic pathways in cancer cells is incompletely understood. On page 975 of this issue, Yi et al. (2) report that modification of the enzyme phosphofructokinase-1 (PFK1) by O-linked β-N-acetylglucosamine (O-GlcNAc) controls its catalytic activity in cancer cells and affects carbon distribution, redox balance, and tumor formation. Unlike most metabolic changes reported in cancer, this mode of regulation appears to be tumor specific.

1 Koch Institute for Integrative Cancer Research and the Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
2 Dana-Farber Cancer Institute, Boston, MA 02115, USA.

E-mail: mvh{at}mit.edu



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