Literature summary for 3.1.3.36 extracted from

Grempler, R.; Zibrova, D.; Schoelch, C.; van Marle, A.; Rippmann, J.F.; Redemann, N.
Normalization of prandial blood glucose and improvement of glucose tolerance by liver-specific inhibition of SH2 domain containing inositol phosphatase 2 (SHIP2) in diabetic KKAy mice: SHIP2 inhibition causes insulin-mimetic effects on glycogen metabolism (2007), Diabetes, 56, 2235-2241.

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Application

Application	Comment	Organism
medicine	inhibition of SHIP2 for the prevention and/or treatment of type 2 diabetes	Mus musculus

Protein Variants

Protein Variants	Comment	Organism
P687A/D691A/R692G	liver-specific expression of a dominant-negative SHIP2 mutant in hyperglycemic and hyperinsulinemic KKAy mice increases basal and insulin-stimulated Akt phosphorylation. Protein levels of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase are reduced, and liver produces less glucose through gluconeogenesis. SHIP2 inhibition improves hepatic glycogen metabolism by modulating the phosphorylation states of glycogen phosphorylase and glycogen synthase, which increases hepatic glycogen content. Enhanced glucokinase and reduced pyruvate dehydrogenase kinase 4 expression, together with increased plasma triglycerides, indicate improved glycolysis. Liver-specific inhibition of SHIP2 improves glucose tolerance and markedly reduces prandial blood glucose levels in KKAy mice	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

Synonyms

Synonyms	Comment	Organism
SH2 domain containing inositol phosphatase 2	-	Mus musculus
SHIP2	-	Mus musculus

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Release 2023.1 (January 2023)