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Publication : Deficiency of a glycogen synthase-associated protein, Epm2aip1, causes decreased glycogen synthesis and hepatic insulin resistance.

First Author  Turnbull J Year  2013
Journal  J Biol Chem Volume  288
Issue  48 Pages  34627-37
PubMed ID  24142699 Mgi Jnum  J:204966
Mgi Id  MGI:5543825 Doi  10.1074/jbc.M113.483198
Citation  Turnbull J, et al. (2013) Deficiency of a glycogen synthase-associated protein, Epm2aip1, causes decreased glycogen synthesis and hepatic insulin resistance. J Biol Chem 288(48):34627-37
abstractText  Glycogen synthesis is a major component of the insulin response, and defective glycogen synthesis is a major portion of insulin resistance. Insulin regulates glycogen synthase (GS) through incompletely defined pathways that activate the enzyme through dephosphorylation and, more potently, allosteric activation. We identify Epm2aip1 as a GS-associated protein. We show that the absence of Epm2aip1 in mice impairs allosteric activation of GS by glucose 6-phosphate, decreases hepatic glycogen synthesis, increases liver fat, causes hepatic insulin resistance, and protects against age-related obesity. Our work identifies a novel GS-associated GS activity-modulating component of insulin resistance.
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