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3.1.3.67: phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase

This is an abbreviated version!
For detailed information about phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase, go to the full flat file.

Word Map on EC 3.1.3.67

Reaction

1-phosphatidyl-1D-myo-inositol 3,4,5-trisphosphate
+
H2O
=
1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
 +
phosphate

Synonyms

1-phosphatidylinositol-3,4,5-trisphosphate 3-phosphohydrolase, MMAC1/TEP1, phosphatase and tensin homolog, phosphatase and tensin homologue, phosphatase and tensin homologue deleted on chromosome 10, phosphatidylinositol 3,4,5-trisphosphate-specific phosphatase, phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase, PI 3-phosphatase, PTEN, PTEN phosphatase, PTEN/MMAC, PTEN/MMAC1, SidF, TPIP, tumor suppressor PREN, voltage-sensing phosphatase, Voltage-sensing phosphoinositide phosphatase, VSP

ECTree

     3 Hydrolases
         3.1 Acting on ester bonds
             3.1.3 Phosphoric-monoester hydrolases
                3.1.3.67 phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase

Cloned

Cloned on EC 3.1.3.67 - phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase

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CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
adenovirus expressing PTEN wild-type, encoding full-length human wild-type PTEN cDNA and AdPTENC/S, encoding a dominant negative human PTEN cDNA mutant (cysteine 124 changed to serine within the catalytic domain) are used for the transduction of cell cultures, overexpression of PTEN and its mutant
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By crossing CD18-Cre recombinase transgenic mice with mice with a conditional point mutation of the pten gene, pten gene is specifically deleted in the B-cell lineage. Mutant animals do not develop B-cell malignancies.
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C-terminal domain of enzyme is expressed in BL21 (DE3) Escherichia coli cells as glutathione S-transferase-protein. Par-3/PDZ3-PTEN peptide single chain fusion protein contains a thrombin cleavage site (LVPRGS) between the C-terminus of PDZ3 domain and the PTEN peptide (DEDQSHQITKV), production of a canine knockdown
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cDNA is subcloned into bicistronic pIRES vector, which also codes for GFP expression and transiently transfected into the following cell lines: HaCaT, MCA3D, NIH 3T3, 3T3 Ki ras and 3T3 v-src
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Conditionally deleted pten in oocytes using transgenic mice expressing Cre recombinase under the control of the growth differentiation factor 9 promoter. Pten deficiency in murine oocytes causes the entire oocyte pool to become activated in life.
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Creating of a conditional mutant with a combined deletion of Smad4 and Pten, the double mutant shows skin tumor onset
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crossing of mice expressing Cre recombinase under the control of the nestin promoter to conditional PTEN mice, mice show a continous increase in brain size throughout embryonal development, individual cells from mutant brain are larger than that of wild type brains
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cytosolic domain (amino acids 215–522) is used for analysis
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cytosolic domain (amino acids 248-576) is used for analysis
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deletion of pten gene in the urothelium results in an increased susceptibility to chemically induced carcinogenesis
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expressed in Escherichia coli
expression in Escherichia coli
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female pten-deficient +/- mice develop multifocal endometrial complex atypical hyperplasia between the age of 18 and 39 weeks
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fusion of a C-terminal truncated PTEN (amino acids 1-378) to Mycobacterium xenopi GyrA intein, and chitin-binding domain
Generating of mice with a complete ablation of PTEN is achieved by crossing mice with a conditional point mutation of the pten gene with two transgenic strains in which Cre recmbinase is under the control of the probasin promoter. Mice with complete loss of PTEN in the prostate show 100% penetrance of invasive prostate cancer starting st the age of 6 month
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Generating of pten +/hyp mice that carry only one hypomorphic pten allele and thus expresses half of the wild type level of one wild type allele. Pten +/hyp mice are crossed with pten +/- mice to generate pten +/+, pten +/-, pten +/hyp and pten hyp/- mice. The pten hyp/- mice are not born at the expected Mendelian ratio, indicating that the hypomorphic pten allele is insufficient to rescue development in all embryos. Surviving male pten hyp/- mice have a much higher incidence of pathological changes in the prostate
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generating of Pten-deficient mice leads to an increasing rate of fatty acid synthesis that is 2.5 times higher than in wild types, furthermore an increase in insulin sensitivity in liver-specifiv Pten-deficient mice is observed, which results in lower fasting plasma glucose levels and reduced serum insulin
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Generating of thyroid-specific PTEN-deficient mice using TpoCre transgenic mice,PTEN deletion does not affect normal thyroid development and function, but may contribute to adenoma development
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generation of mice with conditional inactivation of PTEN in the mammary epithelium using two different MMTV-Cre recombinase mouse strains results in developmental defects of the mammary gland, mammary ducts in the mutant mice grow much faster than in wild type mice and exhibit excessive side branching and precocious lobuloalveolar budding
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GFP-tagged wild-type, C124S and G129E mutant PTEN are constructed
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glioma cell lines U-87MG and U-373MG are stably transfected with wildtype PTEN or catalytically altered mutants of PTEN
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homozygous conditional inactivation of PTEN in endothelial and endocardial cells results in embryonic lethality
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mice heterozygous for a null mutation of pten gene shows a higher risk for the development of breast and endometrial cancers, by 30-49 weeks of age, 61% female PTEN +/- mice have developed mammary tumors that are mainly adenocarcinomas or small fibroadenomas
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mice which deleted pten gene in all T lineage cells show lymphadenopathy, splenomegaly and an enlarged thymus at 6-8 weeks of age, tumor formation is observed from 10 weeks onward and all mice died of malignant T-cell lymphoma by week 17
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mice with a conditional null mutation of the pten gene are crossed to transgenic mice in which Cre recombinase expression is driven by the glial fibrillary acidic protein promoter
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Mutant mice with brain-specific PTEN deficiency are generated. One transgenic mouse strain expressed Cre recombinase under the control of the engrailed-2 promoter. Crossing of this strain to mice with a conditional null mutation of the pten gene results in the inactivation of PTEN in cells that localize to the dorsal midbrain-hindbrain junction and give rise to cells that populate the vermis of the cerebellum.
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overexpressed in 3T3L1 adipocytes
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overexpressed in MCF-7 breast cancer cell line
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PTEN is ligated into the pBacPAK9 baculovirus transfer vector. Sf9 cells are infected with the recombinant PTEN baculovirus
PTEN liver-specific knock-out mice are generated
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PTEN-null U87 cells are transiently transfected with either wild-type PTEN-green fluorescent protein or PTEN-alanine substituted-green fluorescent protein. U87 cells expressing PH-AKT1-green fluorescent protein are co-transfected with either wildtype PTEN or PTEN-alanine substituted enzyme. Whereas two cells co-expressing wild-type PTEN and PH-AKT1-green fluorescent protein fails to respond to epidermal growth factor stimulation, all PTEN-alanine substituted proteins co-transfected cells fail to respond. HeLa cells are transiently co-transfected with cyan fluorescent protein-FKBP-inositol polyphosphate-5-phosphatase and PTEN-C124S-alanine substituted-yellow fluorescent protein. Expression of PTEN-C124Salanine substituted-yellow fluorescent protein in HeLa cells.
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Strain of mice with a prostate-specfic deletion of pten is created using Cre recombinase under the control of the prostate-specific antigen promoter, all mutant mice show prostate hyperplasia with focal PIN at the age of 4-5 months. By 7-9 months, PIN is widespread and focal microinvasion is observed. All mutant mice aged 10-14 months show invasive prostate cancer.
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The cDNA encoding full-length 1-403 PTEN is cloned into the NdeI and XhoI sites of the pET30b vector, thereby introducing a poly-His tag at the C-terminus. Point mutations are introduced with the Quick-Change site-directed mutagenesis kit. Deletion mutant 16-403 is prepared by PCR with the Phusion DNA polymerase. PTEN proteins are expressed in Escherichia coli BL21 (DE3) cells.
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the keratin 5 promotor-cren recombinase-driven deletion of pten gene induces hyperplasia of both skin and esophageal squamous epithelium, the esophageal hyperplasia in malnutrition of pups during lactation, 90% of them died within 21 days of birth
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To explore PTEN function in the liver, two groups cross PTEN mice containing a conditional point mutation, with AlbCre mice, which express Cre recombinase under the control of albumin promoter. Striking hepatomegaly is observed, which progressed with age. Mutants show accumulation of cytoplasmatic triglycerides that expand over time to severe steatohepatits. In addition, inflammatory cell infiltrates are observed in mutant livers at 24 weeks
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transgenic mouse strain expressing Cre recombinase under the control of the L7 promoter, which results in the selective inactivation of PTEN in Purkinje cells
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Wild type and mutant cDNA is subcloned in the vector pcDNA3.1 to generate expression vectors, transduction of recombinant PTEN and PTEN mutant into TMK-1 cells. Recombinant PTEN effectively downregulates phospho-Akt levels as well as the LY294002 phosphatidylinositol 3-kinase inhibitor
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