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Literature summary extracted from

  • Vinciguerra, M.; Foti, M.
    PTEN and SHIP2 phosphoinositide phosphatases as negative regulators of insulin signalling (2006), Arch. Physiol. Biochem., 112, 89-104.
    View publication on PubMed

Application

EC Number Application Comment Organism
3.1.3.36 medicine SHIP2 plays an important role in insulin-dependent signaling pathways controlling glucose and lipid, metabolsim in vivo. A fine tuning of SHIP2 expression/activation in target organs is likely to be beneficial to correct metabolic dysfunctions in pathological conditions such as insulin resistance diabetes melitus and obesity Mus musculus
3.1.3.67 medicine PTEN plays an important role in insulin-dependent signaling pathways controlling glucose and lipid metabolsim in vivo. A fine tuning of PTEN expression/activation in target organs is likely to be beneficial to correct metabolic dysfunctions in pathological conditions such as insulin resistance diabetes melitus and obesity Mus musculus

Cloned(Commentary)

EC Number Cloned (Comment) Organism
3.1.3.36 overexpression of SHIP2 in 3T3-L1 adipocytes, B lymphocytes and L6 myotubes Mus musculus
3.1.3.36 overexpression of SHIP2 in CHO cells Cricetulus griseus
3.1.3.36 overexpression of SHIP2 in COS-7 cells Chlorocebus aethiops
3.1.3.67 overexpressed in 3T3L1 adipocytes Mus musculus
3.1.3.67 overexpressed in MCF-7 breast cancer cell line Homo sapiens

Protein Variants

EC Number Protein Variants Comment Organism
3.1.3.36 additional information direct interaction of SHIP2 with insulin receptor and filamin are evidenced in COS-7 cells Chlorocebus aethiops
3.1.3.36 additional information in CHO cells, SHIP2 is found to form a complex with Cbl and Cbl-associated protein (CAP), two proteins potentially involved in insulin-induced glucose uptake Cricetulus griseus
3.1.3.36 additional information liver-specific overexpresion of wild-type SHIP2 or a dominant-negative mutant in mice by adenoviral vector injection leads to inhibition of insulin-induced Akt activation, glucose metabolism and hepatic gene expression using wild-type SHIP2 while the dominant negative mutant fails to do so Mus musculus
3.1.3.36 additional information overexpression of SHIP2 in L6 myotubes and B lymphocytes results in inhibition of both Akt-dependent and ERK1/2-dependent pathways stimulated by insulin. Expression of a dominant negative SHIP2 mutant in 3T3-L1 adipocytes results in inactivation of insulin signaling through the PI-3 kinase/Akt pathway. However, when SHIP2 is knocked down by RNA silencing in 3T3-L1 adipocytes, no effects are observed, suggesting that loss of SHIP2 function has no impact on insulin singnaling in 3T3-L1 adipocytes Mus musculus
3.1.3.36 additional information SHIP2 knock out mice (deletion of the first 18 exons of the SHIP2 gene) exhibit enhanced PtdIns 3-kinase-dependent signalling, alteration in lipid metabolism and energy expenditure. SHIP2 knock-out mice fed with a high-fat diet are resistant to weight gain and do not become hyperglycemic or insulin resistant Mus musculus
3.1.3.67 additional information adipose tissue-specific depletion of PTEN in mice results in improved glucose tolerance and insulin sensitivity rendering mice resistant to streptozotocin-induced diabetes. Increased recruitment of Glut4 transporters at the plasma membrane of adipocytes,whereas the contrary is observed in muscle of the same animals. Decreased expression of resistin is shown Mus musculus
3.1.3.67 additional information deletion of one PTEN allele in insulin receptor substrate 2 (IRS2) in mice is able to restore pancreatic beta-cell function, peripheral insulin sensitivity, glucose tolerance and significantly increases life span of the animals, indicating that PTEN controls insulin sensitivity in peripheral tissues and pancreatic beta-cell growth and function Mus musculus
3.1.3.67 additional information liver-specific deletion of PTEN in mice results in enhanced insulin sensitivity, hypoinsulinemia, hypoleptinemia and overall improved glucose tolerance. Adult mice lacking PTEN in liver also develop hepatomegaly syndromes, steatohepatitis and hepatocellular carcinomas Mus musculus
3.1.3.67 additional information muscle-specific depletion of PTEN in mice results in improved glucose metabolism in animals with diabetes and insulin resistance. Elevated fasting glucose levels are prevented and insulin sensitivity and glucose tolerance in high-fat fed animals are improved. Insulin stimulated Akt-activation is enhanced. PTEN depletion in muscle is not associated with increased tumorigenesis Mus musculus
3.1.3.67 additional information overexpresion of catalytically inactive or dominant-negative PTEN mutants in 3T1-L1 adipocytes show that it is the lipid phosphatase activity of PTEN which is required to downregulate Akt/PKB signaling and glucose uptake in response to insulin Mus musculus
3.1.3.67 additional information PTEN downregulation in 3T1-L1 adipocytes by small interfering RNAs enhances Akt/PKB activation and glucose uptake in response to insulin Mus musculus
3.1.3.67 additional information PTEN null mutations in mice are lethal at embryonic stages and even a 50% reduction in PTEN expression leads to increased tumorigenesis Mus musculus
3.1.3.67 additional information PTEN overexpression in 3T1-L1 adipocytes causes inhibition of insulin-induced PtdIns(3,4)P2 and PtdIns(3,4,5)P3 production, Akt/PKB activation, GLUT4 translocation to the cell membrane and glucose uptake Mus musculus
3.1.3.67 additional information PTEN overexpression in MCF-7 breast cancer cell line prevents ERK1/2 phosphorylation in response to insulin. Inhibition of ERK1/2 activation is not only caused by a reduction in PtdIns(3,4,5)P3 level but also by a decreased association of Shc with Grb2/Sos complex and Ras activation Homo sapiens

Organism

EC Number Organism UniProt Comment Textmining
3.1.3.36 Chlorocebus aethiops
-
-
-
3.1.3.36 Cricetulus griseus
-
-
-
3.1.3.36 Mus musculus
-
-
-
3.1.3.67 Homo sapiens
-
-
-
3.1.3.67 Mus musculus
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.1.3.36 adipocyte
-
 Mus musculus
-
3.1.3.36 CHO cell
-
 Cricetulus griseus
-
3.1.3.36 COS-7 cell
-
 Chlorocebus aethiops
-
3.1.3.36 liver
-
 Mus musculus
-
3.1.3.36 lymphocyte
-
 Mus musculus
-
3.1.3.36 myotube
-
 Mus musculus
-
3.1.3.67 adipocyte
-
 Mus musculus
-
3.1.3.67 breast cancer cell line
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3.1.3.36 D-myo-phosphatidylinositol 3,4,5-trisphosphate
-
 Cricetulus griseus D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate
-
 ?
3.1.3.36 D-myo-phosphatidylinositol 3,4,5-trisphosphate
-
 Mus musculus D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate
-
 ?
3.1.3.36 D-myo-phosphatidylinositol 3,4,5-trisphosphate
-
 Chlorocebus aethiops D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate
-
 ?
3.1.3.67 1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate + H2O
-
 Mus musculus 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate + phosphate
-
 ?
3.1.3.67 1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate + H2O
-
 Homo sapiens 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate + phosphate
-
 ?
3.1.3.67 phosphatidylinositol 3,4-bisphosphate + H2O
-
 Mus musculus phosphatidylinositol 4-phosphate + phosphate
-
 ?
3.1.3.67 phosphatidylinositol 3,4-bisphosphate + H2O
-
 Homo sapiens phosphatidylinositol 4-phosphate + phosphate
-
 ?

Synonyms

EC Number Synonyms Comment Organism
3.1.3.36 SHIP2
-
 Cricetulus griseus
3.1.3.36 SHIP2
-
 Mus musculus
3.1.3.36 SHIP2
-
 Chlorocebus aethiops
3.1.3.67 PTEN
-
 Mus musculus
3.1.3.67 PTEN
-
 Homo sapiens