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The hexosamine signaling pathway: O-GlcNAc cycling in feast or famine Hanover JA; Krause MW; Love DCBiochim Biophys Acta 2010[Feb]; 1800 (2): 80-95The enzymes of O-GlcNAc cycling couple the nutrient-dependent synthesis of UDP-GlcNAc to O-GlcNAc modification of Ser/Thr residues of key nuclear and cytoplasmic targets. This series of reactions culminating in O-GlcNAcylation of targets has been termed the hexosamine signaling pathway (HSP). The evolutionarily ancient enzymes of O-GlcNAc cycling have co-evolved with other signaling effecter molecules; they are recruited to their targets by many of the same mechanisms used to organize canonic kinase-dependent signaling pathways. This co-recruitment of the enzymes of O-GlcNAc cycling drives a binary switch impacting pathways of anabolism and growth (nutrient uptake) and catabolic pathways (nutrient sparing and salvage). The hexosamine signaling pathway (HSP) has thus emerged as a versatile cellular regulator modulating numerous cellular signaling cascades influencing growth, metabolism, cellular stress, circadian rhythm, and host-pathogen interactions. In mammals, the nutrient-sensing HSP has been harnessed to regulate such cell-specific functions as neutrophil migration, and activation of B-cells and T-cells. This review summarizes the diverse approaches being used to examine O-GlcNAc cycling. It will emphasize the impact O-GlcNAcylation has upon signaling pathways that may be become deregulated in diseases of the immune system, diabetes mellitus, cancer, cardiovascular disease, and neurodegenerative diseases.|Acetylglucosamine/physiology[MESH]|Acetylglucosaminidase/metabolism[MESH]|Animals[MESH]|Caenorhabditis elegans[MESH]|Catalytic Domain[MESH]|Diabetes Mellitus, Type 2/physiopathology[MESH]|Evolution, Molecular[MESH]|Food[MESH]|Gene Expression Regulation/physiology[MESH]|Humans[MESH]|Insulin Resistance/physiology[MESH]|MAP Kinase Signaling System/physiology[MESH]|Models, Animal[MESH]|Models, Molecular[MESH]|N-Acetylglucosaminyltransferases/*metabolism[MESH]|Proteasome Endopeptidase Complex/physiology[MESH]|Proto-Oncogene Proteins c-akt/physiology[MESH]|Sirtuins/physiology[MESH]|Starvation[MESH] |
