|1.||Suzuki, Akira: 3 articles (07/2015 - 04/2003)|
|2.||Gray, Alexander: 3 articles (02/2012 - 02/2010)|
|3.||Erneux, Christophe: 3 articles (11/2011 - 11/2003)|
|4.||Downes, C Peter: 3 articles (04/2010 - 01/2004)|
|5.||Ooms, Lisa M: 2 articles (08/2015 - 01/2007)|
|6.||Mitchell, Christina A: 2 articles (08/2015 - 01/2007)|
|7.||Sasaki, Takehiko: 2 articles (07/2015 - 11/2003)|
|8.||Ijuin, Takeshi: 2 articles (01/2015 - 04/2006)|
|9.||Takenawa, Tadaomi: 2 articles (01/2015 - 04/2006)|
|10.||Vanhaesebroeck, Bart: 2 articles (10/2014 - 02/2012)|
11/15/2003 - "In the present study, we show that SHIP1 and SHIP2 are expressed as functional PtdIns(3,4,5) P3 5-phosphatases in human blood platelets and are capable of interacting when these two lipid phosphatases are co-expressed, either naturally (platelets and A20 B lymphoma cells) or artificially (COS-7 cells). "
11/01/2015 - "Mutating critical SIN1 residues that mediate PtdIns(3,4,5)P3 interaction inactivates mTORC2, whereas mTORC2 activity is pathologically increased by patient-derived mutations in the SIN1-PH domain, promoting cell growth and tumor formation. "
07/01/2015 - "We propose that the PtdIns(3,4,5)P3 phosphatase activity of INPP4B can function as a "back-up" mechanism when PTEN is deficient, making INPP4B a potential novel therapeutic target for PTEN-deficient or PIK3CA-activated cancers. "
07/01/2015 - "Here, we demonstrate that INPP4B restrains tumor development by dephosphorylating the PtdIns(3,4,5)P3 that accumulates in situations of PTEN deficiency. "
07/01/2015 - "INPP4B Is a PtdIns(3,4,5)P3 Phosphatase That Can Act as a Tumor Suppressor."
01/01/2013 - "PTEN is an important tumor suppressor and hydrolyzes PtdIns(3,4,5)P3. "
|3.||Astrocytoma (Pilocytic Astrocytoma)
02/28/1997 - "Measurements on a wide range of cells, including rat-1 fibroblasts, 1321N1 astrocytoma cells, HEK 293 cells, and rat adipocytes, show wortmannin-sensitive increased levels of PtdIns(3,4,5)P3 upon stimulation with appropriate agonists. "
11/01/2011 - "In a model of PTEN (phosphatase and tensin homologue deleted on chromosome 10)-null astrocytoma cells, lowering SHIP2 expression leads to increased PtdIns(3,4,5)P3 levels and Akt phosphorylation. "
07/15/1996 - "Thrombin receptors modulate insulin-stimulated phosphatidylinositol 3,4,5-trisphosphate accumulation in 1321N1 astrocytoma cells."
05/01/2004 - "In 1321N1 astrocytoma cells, stimulation of the IGF-1 (insulin-like growth factor-1) receptor increased the association of PI3K [phosphoinositide (PI) 3-kinase] activity with IRS-1 (insulin re-ceptor substrate 1), and increased the cellular concentration of PtdIns(3,4,5)P3. "
|4.||Oculocerebrorenal Syndrome (Lowe Syndrome)
02/28/1997 - "SIP-110 also hydrolyzed PtdIns(3,4,5)P3 to PtdIns(3,4)P2 as did recombinant forms of two other 5-phosphatases designated as inositol polyphosphate-5- phosphatase II, and OCRL (the protein that is mutated in oculocerebrorenal syndrome). "
05/01/2007 - "Dd5P4 is the Dictyostelium homolog of human OCRL (oculocerebrorenal syndrome of Lowe); both have a RhoGAP domain and a 5-phosphatase domain that acts on phosphatidylinositol 4,5-bisphosphate/phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3). "
01/01/2007 - "Hydrolysis of PtdIns(4,5)P2 and PtdIns(3,4,5)P3, by inositol polyphosphate 5-phosphatases regulates synaptic vesicle recycling (synaptojanin-1), hematopoietic cell function [SHIP1(SH2-containing inositol polyphosphate 5-phosphatase-1)], renal cell function [OCRL (oculocerebrorenal syndrome of Lowe)] and insulin signalling (SHIP2). "
02/02/2010 - "During infection, a recombinant influenza A virus expressing NS1 with charge-disruption mutations in this acidic alpha-helix is unable to stimulate the production of phosphatidylinositol 3,4,5-trisphosphate or the phosphorylation of Akt. "
03/30/2009 - "This analysis revealed increased levels of raft-associated phosphatidylinositol (PI) and phosphorylated PI during RSV infection, which correlated with the appearance of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-triphosphate (PIP(3)) within virus inclusion bodies, and inhibiting the synthesis of PIP(3) impaired the formation of progeny virus. "
01/01/2009 - "Enteropathogenic Escherichia coli subverts phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate upon epithelial cell infection."
|1.||Phosphoric Monoester Hydrolases (Phosphatases)
|5.||PTEN Phosphohydrolase (PTEN Phosphatase)
|8.||Phosphatidylinositol 4,5-Diphosphate (Phosphatidylinositol 4,5 Diphosphate)