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Literature summary for 3.1.3.36 extracted from
- PTEN and SHIP2 phosphoinositide phosphatases as negative regulators of insulin signalling (2006), Arch. Physiol. Biochem., 112, 89-104.
Application
| Application | Comment | Organism |
|---|---|---|
| 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 |
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| overexpression of SHIP2 in 3T3-L1 adipocytes, B lymphocytes and L6 myotubes | Mus musculus |
| overexpression of SHIP2 in CHO cells | Cricetulus griseus |
| overexpression of SHIP2 in COS-7 cells | Chlorocebus aethiops |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | direct interaction of SHIP2 with insulin receptor and filamin are evidenced in COS-7 cells | Chlorocebus aethiops |
| 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 |
| 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 |
| 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 |
| 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 |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Chlorocebus aethiops | - |
- |
- |
| Cricetulus griseus | - |
- |
- |
| Mus musculus | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| adipocyte | - |
Mus musculus | - |
| CHO cell | - |
Cricetulus griseus | - |
| COS-7 cell | - |
Chlorocebus aethiops | - |
| liver | - |
Mus musculus | - |
| lymphocyte | - |
Mus musculus | - |
| myotube | - |
Mus musculus | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| D-myo-phosphatidylinositol 3,4,5-trisphosphate | - |
Cricetulus griseus | D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate | - |
? |  |
| D-myo-phosphatidylinositol 3,4,5-trisphosphate | - |
Mus musculus | D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate | - |
? | |
| D-myo-phosphatidylinositol 3,4,5-trisphosphate | - |
Chlorocebus aethiops | D-myo-phosphatidylinositol 3,4-bisphosphate + phosphate | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| SHIP2 | - |
Cricetulus griseus |
| SHIP2 | - |
Mus musculus |
| SHIP2 | - |
Chlorocebus aethiops |
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Release 2023.1 (January 2023)
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