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- Publisher Website: 10.1247/csf.28.11
- Scopus: eid_2-s2.0-0037310664
- PMID: 12655146
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Article: Physiological functions of Pten in mouse tissues
Title | Physiological functions of Pten in mouse tissues |
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Authors | |
Keywords | Cre-loxP system Tissue-specific mutant mice Pten |
Issue Date | 2003 |
Citation | Cell Structure and Function, 2003, v. 28, n. 1, p. 11-21 How to Cite? |
Abstract | PTEN is a tumor suppressor gene mutated in many human sporadic cancers and in hereditary cancer syndromes such as Cowden disease, Bannayan-Zonana syndrome and Lhermitte-Duclos disease. The major substrate of PTEN is PIP3, a second messenger molecule produced following PI3K activation induced by variety of stimuli. PIP3 activates the serine-threonine kinase PKB/Akt which is involved in anti-apoptosis, proliferation and oncogenesis. In mice, heterozygosity for a null mutation of Pten (Pten+/- mice) frequently leads to the development of a variety of cancers and autoimmune disease. Homozygosity for the null mutation (Pten-/- mice) results in early embryonic lethality, precluding the functional analysis of Pten in various organs. To investigate the physiological functions of Pten in viable mice, various tissue-specific Pten mutations have been generated using the Cre-loxP system. This review will summarize the phenotypes of conditional mutant mice lacking Pten function in specific tissues, and discuss how these phenotypes relate to the physiological roles of Pten in various organ systems. |
Persistent Identifier | http://hdl.handle.net/10722/292520 |
ISSN | 2023 Impact Factor: 2.0 2023 SCImago Journal Rankings: 0.768 |
DC Field | Value | Language |
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dc.contributor.author | Kishimoto, Hiroyuki | - |
dc.contributor.author | Hamada, Koichi | - |
dc.contributor.author | Saunders, Mary | - |
dc.contributor.author | Backman, Stephanie | - |
dc.contributor.author | Sasaki, Takehiko | - |
dc.contributor.author | Nakano, Toru | - |
dc.contributor.author | Mak, Tak Wah | - |
dc.contributor.author | Suzuki, Akira | - |
dc.date.accessioned | 2020-11-17T14:56:39Z | - |
dc.date.available | 2020-11-17T14:56:39Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Cell Structure and Function, 2003, v. 28, n. 1, p. 11-21 | - |
dc.identifier.issn | 0386-7196 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292520 | - |
dc.description.abstract | PTEN is a tumor suppressor gene mutated in many human sporadic cancers and in hereditary cancer syndromes such as Cowden disease, Bannayan-Zonana syndrome and Lhermitte-Duclos disease. The major substrate of PTEN is PIP3, a second messenger molecule produced following PI3K activation induced by variety of stimuli. PIP3 activates the serine-threonine kinase PKB/Akt which is involved in anti-apoptosis, proliferation and oncogenesis. In mice, heterozygosity for a null mutation of Pten (Pten+/- mice) frequently leads to the development of a variety of cancers and autoimmune disease. Homozygosity for the null mutation (Pten-/- mice) results in early embryonic lethality, precluding the functional analysis of Pten in various organs. To investigate the physiological functions of Pten in viable mice, various tissue-specific Pten mutations have been generated using the Cre-loxP system. This review will summarize the phenotypes of conditional mutant mice lacking Pten function in specific tissues, and discuss how these phenotypes relate to the physiological roles of Pten in various organ systems. | - |
dc.language | eng | - |
dc.relation.ispartof | Cell Structure and Function | - |
dc.subject | Cre-loxP system | - |
dc.subject | Tissue-specific mutant mice | - |
dc.subject | Pten | - |
dc.title | Physiological functions of Pten in mouse tissues | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1247/csf.28.11 | - |
dc.identifier.pmid | 12655146 | - |
dc.identifier.scopus | eid_2-s2.0-0037310664 | - |
dc.identifier.volume | 28 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 11 | - |
dc.identifier.epage | 21 | - |
dc.identifier.issnl | 0386-7196 | - |