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These data show that G6P-mediated activation of GYS2 plays a key role in controlling glycogen synthesis and hepatic glucose-G6P flux control and thus whole-body glucose homeostasis.
A stratified transcriptomics analysis of polygenic fat and lean mouse adipose tissues identifies Gys2 as novel candidate obesity genes.
Transgenic LGS (show LGSN Proteins) mice showed enhanced glycogen (show GYS1 Proteins) storage and an mproved glucose tolerance.
CLOCK regulates the circadian rhythms of hepatic glycogen (show GYS1 Proteins) synthesis through transcriptional activation of Gys2.
The endogenous glycogen synthase in extracts from mouse liver bound specifically to SAPK2b/p38b (show MAPK11 Proteins) & was phosphorylated at residues Ser644, Ser652, Thr718 and Ser724.
Mouse enzyme is a novel target of peroxisome proliferator-activated receptor (show PPARG Proteins), which is in turn mediated by two response elements.
Sequencing of the GYS2 gene is more likely to be positive in patients with fasting ketotic hypoglycaemia and concomitant postprandial hyperglycaemia with hyperlactataemia.
The GYS2 gene is a new susceptibility gene that significantly affects the risk for ovary syndrome through obesity-related conditions.
GYS2 was expressed specifically in liver and subcutaneous adipose tissue
The protein encoded by this gene, liver glycogen synthase, catalyzes the rate-limiting step in the synthesis of glycogen - the transfer of a glucose molecule from UDP-glucose to a terminal branch of the glycogen molecule. Mutations in this gene cause glycogen storage disease type 0 (GSD-0) - a rare type of early childhood fasting hypoglycemia with decreased liver glycogen content.
glycogen [starch] synthase, liver
, glycogen synthase, liver
, Glycogen synthase 2 (liver)