EC Number   |
General Information |
Reference |
|---|
   3.1.3.36 | malfunction |
in SKIP siRNA transfected cells, insulin treatment show an increase in PIP3 compared with control cells. Significant decrease in PI(3,4)P2 level is observed by the silencing of SKIP compared to control cells. PI(3,4)P2 levels are not altered in siRNA-transfected cells. Silencing of SKIP, increases the insulin-dependent recruitment of GLUT4 vesicles to the plasma membrane |
732083 |
| 3.1.3.36 | malfunction |
inactivation of OCRL by siRNA leads to an increase in the internalization levels of Listeria monocytogenes in HeLa cells. OCRL depletion does not increase but rather decreases the surface expression of the receptor Met |
732045 |
| 3.1.3.36 | malfunction |
inducible reduction of negative charge rescues DELTAsopB bacteria-containing Salmonella-containing vacuoles from fusion with lysosomes |
714675 |
| 3.1.3.36 | 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 |
729995 |
| 3.1.3.36 | malfunction |
mutant sac9-1 plants have a constitutively stressed phenotype with shorter roots which notably accumulate phosphatidylinositol 4,5-bisphosphate and its hydrolysis product inositol trisphosphate, phenotype with extreme abnormalities of cell wall and membrane structures in sac9-1 primary root cells, regardless of cell type, position within the meristematic area, and plane of section, overview |
-, 716657 |
| 3.1.3.36 | malfunction |
mutations of isoform OCRL are related to Lowes syndrome and Dent disease characterized by renal failure |
730981 |
| 3.1.3.36 | malfunction |
no effects by siRNA-mediated OCRL1 knockdown on biosynthetic and postendocytic membrane traffic in renal epithelial cells, overview. Cells depleted of OCRL1 do not have significantly elevated levels of cellular PIP2 but display an increase in actin comet, OCRL1 knockdown results in a significant increase in secretion of the lysosomal hydrolase cathepsin D |
713723 |
| 3.1.3.36 | malfunction |
plasma membrane phosphatidylinositol-4,5-bisphosphate depletion by rapamycin-induced translocation of an inositol lipid 5-phosphatase or by a voltage-sensitive 5-phosphatase suppresses CaV1.2 and CaV1.3 channel currents by about 35% and CaV2.1 and CaV2.2 currents by 29% and 55%, respectively, mechanism, detailed overview. Other CaV channels are less sensitive. Inhibition of CaV channels by Dr-VSP is not simple voltage-dependent inhibition. Phosphatidylinositol-4,5-bisphosphate-dependent modulation of CaV2.2 channels and recovery requiring ATP and phosphatidylinositol-4,5-bisphosphate resynthesis, overview |
716345 |
| 3.1.3.36 | malfunction |
reduction of plasma membrane phosphatidylinositol 4,5-bisphosphate by low-level expression of the PIP2 phosphatase SigD or mutation of the PIP2 biosynthetic enzyme Skittles results in dramatic defects in spermatid cysts, which become bipolar and fail to fully elongate |
716164 |
| 3.1.3.36 | malfunction |
SHIP1-/- neutrophils are extremely adherent, which results in impaired cell migration. Reduction in cell adhesion can rescue the defect in cell migration in SHIP1-/- neutrophils. Cell adhesion results in excessive Akt activation in SHIP1-/- cells |
732476 |
