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1. Tuberin, p27 and mTOR in different cells

Author

C. Lindengrün, S. Burgstaller, Marsha Rich Rosner, M. Hanneder, Markus Hengstschläger, Nicol Siegel, Alessandro Valli, and Christiane Fuchs

Subjects
Clinical Biochemistry, P70-S6 Kinase 1, Biology, Biochemistry, mTORC2, Tuberous Sclerosis Complex 1 Protein, Cell Line, Tubulin, Cell Line, Tumor, Tuberous Sclerosis Complex 2 Protein, medicine, Humans, Cyclin D1, PI3K/AKT/mTOR pathway, TOR Serine-Threonine Kinases, Tumor Suppressor Proteins, Organic Chemistry, RPTOR, Intracellular Signaling Peptides and Proteins, Ribosomal Protein S6 Kinases, 70-kDa, Epithelial Cells, Fibroblasts, Cell biology, Isoenzymes, medicine.anatomical_structure, DNA Topoisomerases, Type I, Ribosomal protein s6, Cancer research, biology.protein, TSC1, TSC2, Protein Kinases, Cyclin-Dependent Kinase Inhibitor p27, RHEB, Signal Transduction
Abstract

Mutations in the genes TSC1 or TSC2 cause the autosomal dominantly inherited tumor suppressor syndrome tuberous sclerosis, which is characterized by the development of tumors, named hamartomas, in different organs. The TSC gene products, hamartin and tuberin, form a complex, of which tuberin is assumed to be the functional component. Both, hamartin and tuberin have been implicated in the control of the cell cycle by activating the cyclin-dependent kinase inhibitor p27 and in cell size regulation by inhibiting the mammalian target of rapamycin (mTOR) a regulator of the p70 ribosomal protein S6 kinase (p70S6K) and its target the ribosomal protein S6. The tuberin/hamartin complex was shown to protect p27 from protein degradation. Within the mTOR signaling pathway tuberin harbors GTPase activating (GAP) potential toward Rheb, which is a potent regulator of mTOR. In this study, we have analyzed the protein levels of tuberin, p27, cyclin D1, mTOR and phospho mTOR Ser2448 (activated mTOR), S6 and phospho S6 Ser240/244 (activated S6) and as controls alpha-tubulin and topoisomerase IIbeta, in ten different cells, including primary normal cells, immortalized and transformed cell lines.

Published
2008

2. Tuberin, p27 and mTOR in different cells.

Author

Burgstaller S, Rosner M, Lindengrün C, Hanneder M, Siegel N, Valli A, Fuchs C, and Hengstschläger M

Subjects
Cell Line, Cell Line, Tumor, Cyclin D1 metabolism, Cyclin-Dependent Kinase Inhibitor p27, DNA Topoisomerases, Type I metabolism, Epithelial Cells metabolism, Fibroblasts metabolism, Humans, Isoenzymes metabolism, Ribosomal Protein S6 Kinases, 70-kDa metabolism, Signal Transduction, TOR Serine-Threonine Kinases, Tuberous Sclerosis Complex 1 Protein, Tuberous Sclerosis Complex 2 Protein, Tubulin metabolism, Intracellular Signaling Peptides and Proteins metabolism, Protein Kinases biosynthesis, Tumor Suppressor Proteins biosynthesis
Abstract

Mutations in the genes TSC1 or TSC2 cause the autosomal dominantly inherited tumor suppressor syndrome tuberous sclerosis, which is characterized by the development of tumors, named hamartomas, in different organs. The TSC gene products, hamartin and tuberin, form a complex, of which tuberin is assumed to be the functional component. Both, hamartin and tuberin have been implicated in the control of the cell cycle by activating the cyclin-dependent kinase inhibitor p27 and in cell size regulation by inhibiting the mammalian target of rapamycin (mTOR) a regulator of the p70 ribosomal protein S6 kinase (p70S6K) and its target the ribosomal protein S6. The tuberin/hamartin complex was shown to protect p27 from protein degradation. Within the mTOR signaling pathway tuberin harbors GTPase activating (GAP) potential toward Rheb, which is a potent regulator of mTOR. In this study, we have analyzed the protein levels of tuberin, p27, cyclin D1, mTOR and phospho mTOR Ser2448 (activated mTOR), S6 and phospho S6 Ser240/244 (activated S6) and as controls alpha-tubulin and topoisomerase IIbeta, in ten different cells, including primary normal cells, immortalized and transformed cell lines.

Published
2009
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