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Literature summary for 3.1.3.86 extracted from
- SH2 domain-containing inositol 5-phosphatase (SHIP2) inhibition ameliorates high glucose-induced de-novo lipogenesis and VLDL production through regulating AMPK/mTOR/SREBP1 pathway and ROS production in HepG2 cells (2015), Free Radic. Biol. Med., 89, 679-689 .
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | O15357 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| Hep-G2 cell | - |
Homo sapiens | - |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| SHIP2 | - |
Homo sapiens |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | high glucose induces SHIP2 mRNA and protein levels in HepG2 cells. Overexpression of a dominant negative mutant SHIP2 ameliorates high glucose-induced de novo lipogenesis and secretion of apoB containing lipoprotein in HepG2 cells. Overexpression of the SHIP2 dominant negative mutant decreases high glucose-induced apoB containing lipoproteins secretion via reduction in reactive oxygen species generation, JNK phosphorylation and Akt activation. AMPK/mTOR/SREBP1 is the signaling pathway that mediates the effects of SHIP2 modulation on hepatic de novo lipogenesis | Homo sapiens |
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Release 2023.1 (January 2023)
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