Any feedback?
Literature summary for 3.1.3.67 extracted from
- The roles of PTEN in development, physiology and tumorigenesis in mouse models: a tissue-by-tissue survey (2008), Oncogene, 27, 5398-5415.
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| 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. | Mus musculus |
| 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. | Mus musculus |
| Creating of a conditional mutant with a combined deletion of Smad4 and Pten, the double mutant shows skin tumor onset | Mus musculus |
| 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 | Mus musculus |
| deletion of pten gene in the urothelium results in an increased susceptibility to chemically induced carcinogenesis | Mus musculus |
| female pten-deficient +/- mice develop multifocal endometrial complex atypical hyperplasia between the age of 18 and 39 weeks | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| homozygous conditional inactivation of PTEN in endothelial and endocardial cells results in embryonic lethality | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| 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. | Mus musculus |
| 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. | Mus musculus |
| 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 | Mus musculus |
| 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 | Mus musculus |
| transgenic mouse strain expressing Cre recombinase under the control of the L7 promoter, which results in the selective inactivation of PTEN in Purkinje cells | Mus musculus |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | Mus musculus | depending on the cell type, PTEN is important for proper development, cell fate and cell function, as well as for protection from tumorigenesis | ? | - |
? |  |
| additional information | Mus musculus | lung-specific deletion of PTEN after birth results in bronchiolar and alveolar epithelial hyperplasia | ? | - |
? | |
| additional information | Mus musculus | PTEN acts as an major tumor suppressor gene that is inacitvated in a wide variety of cancers | ? | - |
? | |
| additional information | Mus musculus | PTEN inactivation in pancreas results in increases insulin sensitivity and hypoglycemia and may result in cystic changes of this organ due to mucinous metaplasia. Thus, PTEN is important for the physiological function of the pancreas as well as for the conservation of normal organ structure | ? | - |
? | |
| additional information | Mus musculus | PTEN is critical for insulin regulation and liver homeostasis under physiological conditions, and plays an important role in suppressing the devlopment of hepatic adenomas and hepatocellular carcinomas | ? | - |
? | |
| additional information | Mus musculus | PTEN is required for both maturation and activation of natural killer cells | ? | - |
? | |
| additional information | Mus musculus | PTEN negatively regulates the phosphorylation of the important cellsurvival kinase Akt | ? | - |
? | |
| additional information | Mus musculus | PTEN plays a role in controlling seum insulin and resistin levels, which in turn regulate insulin sensitivity and AMP kinase activity in the liver | ? | - |
? | |
| additional information | Mus musculus | PTEN plays a role in embryogenesis and in maintenance of the normal physiological functions of many organ systems | ? | - |
? | |
| additional information | Mus musculus | PTEN plays an important role for protection from both epithelial as well as melanocytic tumor formation in the skin | ? | - |
? | |
| additional information | Mus musculus | PTEN signaling in Pimc neurons in the hypothlamus is vital for the regulation of food uptake and body weight | ? | - |
? | |
| phosphatidylinositol 3,4,5-triphosphate + H2O | Mus musculus | - |
phosphatidylinositol 4,5-bisphosphate + phosphate | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| adipocyte | - |
Mus musculus | - |
| adrenal gland | - |
Mus musculus | - |
| B-lymphocyte | - |
Mus musculus | - |
| bladder | - |
Mus musculus | - |
| bone | - |
Mus musculus | - |
| brain | - |
Mus musculus | - |
| breast | - |
Mus musculus | - |
| cardiac myocyte | - |
Mus musculus | - |
| cartilage | - |
Mus musculus | - |
| endocardium | - |
Mus musculus | - |
| endothelium | - |
Mus musculus | - |
| gastrointestinal tract | - |
Mus musculus | - |
| granulocyte | - |
Mus musculus | - |
| hematopoietic stem cell | - |
Mus musculus | - |
| hypothalamus | - |
Mus musculus | - |
| keratinocyte | - |
Mus musculus | - |
| liver | - |
Mus musculus | - |
| lung | - |
Mus musculus | - |
| macrophage | - |
Mus musculus | - |
| melanocyte | - |
Mus musculus | - |
| natural killer cell | - |
Mus musculus | - |
| oligodendrocyte | - |
Mus musculus | - |
| oocyte | - |
Mus musculus | - |
| pancreas | - |
Mus musculus | - |
| primordium | - |
Mus musculus | - |
| prostate | - |
Mus musculus | - |
| skeletal muscle | - |
Mus musculus | - |
| smooth muscle | - |
Mus musculus | - |
| T-lymphocyte | - |
Mus musculus | - |
| thyroid gland | - |
Mus musculus | - |
| uterine endometrium | - |
Mus musculus | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | depending on the cell type, PTEN is important for proper development, cell fate and cell function, as well as for protection from tumorigenesis | Mus musculus | ? | - |
? | |
| additional information | lung-specific deletion of PTEN after birth results in bronchiolar and alveolar epithelial hyperplasia | Mus musculus | ? | - |
? | |
| additional information | PTEN acts as an major tumor suppressor gene that is inacitvated in a wide variety of cancers | Mus musculus | ? | - |
? | |
| additional information | PTEN inactivation in pancreas results in increases insulin sensitivity and hypoglycemia and may result in cystic changes of this organ due to mucinous metaplasia. Thus, PTEN is important for the physiological function of the pancreas as well as for the conservation of normal organ structure | Mus musculus | ? | - |
? | |
| additional information | PTEN is critical for insulin regulation and liver homeostasis under physiological conditions, and plays an important role in suppressing the devlopment of hepatic adenomas and hepatocellular carcinomas | Mus musculus | ? | - |
? | |
| additional information | PTEN is required for both maturation and activation of natural killer cells | Mus musculus | ? | - |
? | |
| additional information | PTEN negatively regulates the phosphorylation of the important cellsurvival kinase Akt | Mus musculus | ? | - |
? | |
| additional information | PTEN plays a role in controlling seum insulin and resistin levels, which in turn regulate insulin sensitivity and AMP kinase activity in the liver | Mus musculus | ? | - |
? | |
| additional information | PTEN plays a role in embryogenesis and in maintenance of the normal physiological functions of many organ systems | Mus musculus | ? | - |
? | |
| additional information | PTEN plays an important role for protection from both epithelial as well as melanocytic tumor formation in the skin | Mus musculus | ? | - |
? | |
| additional information | PTEN signaling in Pimc neurons in the hypothlamus is vital for the regulation of food uptake and body weight | Mus musculus | ? | - |
? | |
| phosphatidylinositol 3,4,5-triphosphate + H2O | - |
Mus musculus | phosphatidylinositol 4,5-bisphosphate + phosphate | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| phosphatase and tensin homologue deleted on chromosome 10 | - |
Mus musculus |
| PTEN | - |
Mus musculus |
Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.
Release 2023.1 (January 2023)
Legal
Curated at
Member of
