Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume 1761, Issue 5-6, Pages 599-617Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbalip.2006.04.007
Keywords
metabolic sensor; signal transduction; cellular stress; post-translational modification; O-GlcNAc
Funding
- NCI NIH HHS [R01-CA42486] Funding Source: Medline
- NHLBI NIH HHS [N01-HV28180] Funding Source: Medline
- NICHD NIH HHS [R37-HD13563] Funding Source: Medline
- NIDDK NIH HHS [R01-DK61671, R21/33-DK71280] Funding Source: Medline
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An increasing body of evidence points to a central regulatory role for glucose in mediating cellular processes and expands the role of glucose well beyond its traditional role(s) in energy metabolism. Recently, it has been recognized that one downstream effector produced from glucose is LTDP-GlcNAc. Levels of UDP-GlcNAc, and the subsequent addition of O-linked beta-N-acetylglucosamine (O-GlcNAc) to Ser/Thr residues, is involved in regulating nuclear and cytoplasmic proteins in a manner analogous to protein phosphorylation. O-GlcNAc protein modification is essential for life in mammalian cells, highlighting the importance of this simple post-translational modification in basic cellular regulation. Recent research has highlighted key roles for O-GlcNAc serving as a nutrient sensor in regulating insulin signaling, the cell cycle, and calcium handling, as well as the cellular stress response. (c) 2006 Elsevier B.V. All rights reserved.
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