3.1.3.36	malfunction	At5PTase7 mutants show reduced salt tolerance and increased salt stress response, phenotype, overview	716624	
3.1.3.36	malfunction	both knockdown of SHIP2 expression and acute production of PI(3,4,5)P3 shorten clathrin-coated pits lifetime by enhancing the rate of pit maturation	715707	
3.1.3.36	malfunction	depletion of SHIP2 attenuates cell polarization and migration, which is rescued by wild-type SHIP2 but not by a mutant defective in RhoA binding. In addition, the depletion of SHIP2 impairs the proper localization of phosphatidylinositol 3,4,5-trisphosphate, which is not restored by a mutant defective in RhoA binding	732478	
3.1.3.36	malfunction	enzyme depletion exclusively impairs apical secretory transport in intestinal epithelia. Enzyme loss leads to increased phosphatidylinositol 4,5-bisphosphate levels and overaccumulation of actin structures as well as intracellular accumulation of ARF-6 and UNC-16	751176	
3.1.3.36	malfunction	enzyme knockdown results in increased proliferation and anchorage-independent growth of melanocytes	730456	
3.1.3.36	malfunction	excess amounts of SHIP2 may be related, at least in part, to brain dysfunction in insulin resistance with type 2 diabetes. A dominant-negative mutant of SHIP2, expressed in cultured neurons, causes insulin signaling augmentation. Inhibition of SHIP2 ameliorates the impairment of hippocampal synaptic plasticity and memory formation in db/db mice	-, 716225	
3.1.3.36	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	729995	
3.1.3.36	malfunction	in absence of dOCRL, several essential components of the cleavage furrow are found to be incorrectly localized on giant cytoplasmic vacuoles rich in PI(4,5)P2 and in endocytic markers	714782	
3.1.3.36	malfunction	in cells knocked down for OCRL, transfection of enzymatically active EGFP-OCRL-a (but not of a phosphatase-dead enzyme) decreases the levels of intracellular Listeria monocytogenes and of actin associated with invading bacteria	732045	
3.1.3.36	malfunction	in SHIP2 siRNA transfected cells, insulin treatment does not lead to alter the PIP3 level in contrast to SKIP or PTEN silenced cells. Results demonstrate that SHIP2 in contrast to SKIP is not involved in the regulation of insulin signaling in C2C12 cells	732083