Portrait of PTEN: messages from mutant mice.

@article{citeulike:2744035, abstract = {PTEN is a tumor suppressor gene mutated in many human sporadic cancers and in hereditary cancer syndromes such as Cowden disease. The major substrate of PTEN is phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3), a second messenger molecule produced following PI3K activation induced by a variety of stimuli. PI(3,4,5)P3 activates the serine-threonine kinase Akt, which is involved in antiapoptosis, 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 adult tissues and organs. To investigate the physiological functions of Pten in viable mice, we and other groups have used the Cre-loxP system to generate various tissue-specific Pten mutations. The present review will summarize results obtained from the study of conditional mutant mice lacking Pten in specific tissues, and discuss the possible biological and molecular explanations for why Pten deficiency leads to tumorigenesis.}, address = {Division of Embryonic and Genetic Engineering, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. suzuki@bioreg.kyushu-u.ac.jp}, author = {Suzuki, A. and Nakano, T. and Mak, T. W. and Sasaki, T. }, citeulike-article-id = {2744035}, doi = {10.1111/j.1349-7006.2007.00670.x}, issn = {1349-7006}, journal = {Cancer science}, month = {February}, number = {2}, pages = {209--213}, posted-at = {2008-05-02 05:18:30}, priority = {2}, title = {Portrait of PTEN: messages from mutant mice.}, url = {http://dx.doi.org/10.1111/j.1349-7006.2007.00670.x}, volume = {99}, year = {2008} }

TY - JOUR ID - citeulike:2744035 L3 - citeulike-article-id:2744035 TI - Portrait of PTEN: messages from mutant mice. JF - Cancer science VL - 99 IS - 2 SP - 209 EP - 213 AD - Division of Embryonic and Genetic Engineering, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. suzuki@bioreg.kyushu-u.ac.jp SN - 1349-7006 N2 - PTEN is a tumor suppressor gene mutated in many human sporadic cancers and in hereditary cancer syndromes such as Cowden disease. The major substrate of PTEN is phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3), a second messenger molecule produced following PI3K activation induced by a variety of stimuli. PI(3,4,5)P3 activates the serine-threonine kinase Akt, which is involved in antiapoptosis, 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 adult tissues and organs. To investigate the physiological functions of Pten in viable mice, we and other groups have used the Cre-loxP system to generate various tissue-specific Pten mutations. The present review will summarize results obtained from the study of conditional mutant mice lacking Pten in specific tissues, and discuss the possible biological and molecular explanations for why Pten deficiency leads to tumorigenesis. AU - Suzuki, A AU - Nakano, T AU - Mak, TW AU - Sasaki, T PY - 2008/02// UR - http://dx.doi.org/10.1111/j.1349-7006.2007.00670.x ER -