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Literature summary for 3.1.3.36 extracted from

  • Ijuin, T.; Takenawa, T.
    Role of phosphatidylinositol 3,4,5-trisphosphate (PIP3) 5-phosphatase skeletal muscle- and kidney-enriched inositol polyphosphate phosphatase (SKIP) in myoblast differentiation (2012), J. Biol. Chem., 287, 31330-31341.
    View publication on PubMedView publication on EuropePMC
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Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate + H2O Homo sapiens
-
 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate + phosphate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
C2C12 cell
-
 Mus musculus
-
C2C12 cell
-
 Homo sapiens
-
kidney
-
 Homo sapiens
-
skeletal muscle
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate + H2O
-
 Homo sapiens 1-phosphatidyl-1D-myo-inositol 3,4-bisphosphate + phosphate
-
 ?

Synonyms

Synonyms Comment Organism
phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase
-
 Homo sapiens
PIP3 5-phosphatase
-
 Homo sapiens
skeletal muscle- and kidney-enriched inositol polyphosphate phosphatase
-
 Homo sapiens
SKIP
-
 Mus musculus
SKIP
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens enzyme expression, which is markedly elevated during cell differentiation up
Mus musculus SKIP expression is markedly elevated during differentiation and is controlled by MyoD in C2C12 cells up

General Information

General Information Comment Organism
malfunction knockdown of SKIP results in thick myotubes with a larger number of nuclei than that in control cells and enhances the expression of myogenin mRNA Homo sapiens
malfunction expression of SKIP in C2C12 cells results in a slight decrease in myogenin expression and Akt phosphorylation after 48 h, with a marked decrease in MHC expression after 72 h. Expression of a phosphatase dead mutant in C2C12 cells does not show any effect Mus musculus
malfunction silencing of SKIP increases IGF-II transcription and myoblast differentiation. Knockdown of SKIP results in thick myotubes with a larger number of nuclei than in control C2C12 cells Mus musculus
metabolism the enzyme negatively regulates myogenesis through inhibition of insulin-like growth factor-II production and attenuation of the insulin-like growth factor-II-Akt-mTOR signaling pathway Homo sapiens
physiological function the enzyme regulates MyoD-mediated muscle differentiation Homo sapiens
physiological function SKIP negatively regulates myogenesis through inhibition of IGF-II production and attenuation of the IGF-II-Akt-mTOR signaling pathway. SKIP as a key regulator of muscle cell differentiation Mus musculus