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mTOR Complex 2 Is Required for the Development of Prostate Cancer Induced by Pten Loss in Mice
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“Inhibition of mTORC2 signaling extends the lifespan of C. elegans under certain temperatures and dietary conditions111,112, has anti-tumor effects 128–131, is beneficial in mouse models of mitochondrial disease132,133, and has been shown to inhibit or reverse senescence in human cells 134,135.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [128]
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“The SAMTOR protein acts as an indirect sensor of methionine levels, inhibiting GATOR1 when levels of the methionine metabolite S-adenosylmethionine (SAM) are low (128). As SAM is extremely responsive to methionine levels, SAMTOR essentially functions as a sensor of methionine levels 172.”
From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [128]
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Cites
Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex
Sarbassov, D. D., Guertin, D. A., Ali, S. M., & Sabatini, D. M. (2005) · Science · doi:10.1126/science.1106148 · Cited by 6,216
Self-citationPRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase
Sancak, Y., Thoreen, C. C., Peterson, T. R., Lindquist, R. A., Kang, S. A., Spooner, E., Carr, S. A., & Sabatini, D. M. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.03.003 · Cited by 1,236
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Research works printed but not linked: 53
- Abraham, 2008, Mammalian target of rapamycin as a therapeutic target in oncology, Expert Opin. Ther. Targets, 12, 209, 10.1517/14728222.12.2.209 · DOI
- Alessi, 1996, Mechanism of activation of protein kinase B by insulin and IGF-1, EMBO J., 15, 6541, 10.1002/j.1460-2075.1996.tb01045.x · DOI
- Backman, 2001, Deletion of Pten in mouse brain causes seizures, ataxia and defects in soma size resembling Lhermitte-Duclos disease, Nat. Genet., 29, 396, 10.1038/ng782 · DOI
- Bayascas, 2005, Hypomorphic mutation of PDK1 suppresses tumorigenesis in PTEN(+/−) mice, Curr. Biol., 15, 1839, 10.1016/j.cub.2005.08.066 · DOI
- Bhaskar, 2007, The two TORCs and Akt, Dev. Cell, 12, 487, 10.1016/j.devcel.2007.03.020 · DOI · Paper page
- Biondi, 2001, The PIF-binding pocket in PDK1 is essential for activation of S6K and SGK, but not PKB, EMBO J., 20, 4380, 10.1093/emboj/20.16.4380 · DOI · Paper page
- Bjornsti, 2004, The TOR pathway: a target for cancer therapy, Nat. Rev. Cancer, 4, 335, 10.1038/nrc1362 · DOI
- Bozulic, 2008, PKBalpha/Akt1 acts downstream of DNA-PK in the DNA double-strand break response and promotes survival, Mol. Cell, 30, 203, 10.1016/j.molcel.2008.02.024 · DOI
- Chen, 2006, The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/− mice, Genes Dev., 20, 1569, 10.1101/gad.1395006 · DOI
- Chiang, 2007, Targeting the mTOR signaling network in cancer, Trends Mol. Med., 13, 433, 10.1016/j.molmed.2007.08.001 · DOI
- Collins, 2003, In vivo role of the PIF-binding docking site of PDK1 defined by knock-in mutation, EMBO J., 22, 4202, 10.1093/emboj/cdg407 · DOI
- Dahia, 2000, PTEN, a unique tumor suppressor gene, Endocr. Relat. Cancer, 7, 115, 10.1677/erc.0.0070115 · DOI
- Di Cristofano, 1998, Pten is essential for embryonic development and tumour suppression, Nat. Genet., 19, 348, 10.1038/1235 · DOI
- Facchinetti, 2008, The mammalian target of rapamycin complex 2 controls folding and stability of Akt and protein kinase C, EMBO J., 27, 1932, 10.1038/emboj.2008.120 · DOI
- Freeman, 2006, Genetic background controls tumor development in PTEN-deficient mice, Cancer Res., 66, 6492, 10.1158/0008-5472.CAN-05-4143 · DOI
- Frias, 2006, mSin1 is necessary for Akt/PKB phosphorylation, and its isoforms define three distinct mTORC2s, Curr. Biol., 16, 1865, 10.1016/j.cub.2006.08.001 · DOI
- Garcia-Martinez, 2008, mTOR complex-2 (mTORC2) controls hydrophobic motif phosphorylation and activation of serum and glucocorticoid induced protein kinase-1 (SGK1), Biochem. J., 416, 375, 10.1042/BJ20081668 · DOI · Paper page
- Guertin, 2007, Defining the Role of mTOR in Cancer, Cancer Cell, 12, 9, 10.1016/j.ccr.2007.05.008 · DOI · Paper page
- Guertin, 2006, Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1, Dev. Cell, 11, 859, 10.1016/j.devcel.2006.10.007 · DOI
- Hanada, 2004, Structure, regulation and function of PKB/AKT--a major therapeutic target, Biochim. Biophys. Acta, 1697, 3, 10.1016/j.bbapap.2003.11.009 · DOI
- Hietakangas, 2007, Re-evaluating AKT regulation: role of TOR complex 2 in tissue growth, Genes Dev., 21, 632, 10.1101/gad.416307 · DOI
- Hresko, 2005, mTOR/RICTOR is the Ser473 kinase for Akt/protein kinase B in 3T3-L1 adipocytes, J. Biol. Chem., 280, 40406, 10.1074/jbc.M508361200 · DOI
- Huang, 2005, Expression of proline-rich Akt-substrate PRAS40 in cell survival pathway and carcinogenesis, Acta Pharmacol. Sin., 26, 1253, 10.1111/j.1745-7254.2005.00184.x · DOI
- Ikenoue, 2008, Essential function of TORC2 in PKC and Akt turn motif phosphorylation, maturation and signalling, EMBO J., 27, 1919, 10.1038/emboj.2008.119 · DOI
- Jacinto, 2006, SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity, Cell, 127, 125, 10.1016/j.cell.2006.08.033 · DOI
- Jiao, 2007, Murine cell lines derived from Pten null prostate cancer show the critical role of PTEN in hormone refractory prostate cancer development, Cancer Res., 67, 6083, 10.1158/0008-5472.CAN-06-4202 · DOI
- Kim, 2002, mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery, Cell, 110, 163, 10.1016/S0092-8674(02)00808-5 · DOI
- Kovacina, 2003, Identification of a proline-rich Akt substrate as a 14-3-3 binding partner, J. Biol. Chem., 278, 10189, 10.1074/jbc.M210837200 · DOI
- Kumar, 2008, Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances basal glycogen synthase activity, Mol. Cell. Biol., 28, 61, 10.1128/MCB.01405-07 · DOI
- Lee, 2005, TOR complex 2 integrates cell movement during chemotaxis and signal relay in Dictyostelium, Mol. Biol. Cell, 16, 4572, 10.1091/mbc.e05-04-0342 · DOI
- Lei, 2006, NKX3.1 stabilizes p53, inhibits AKT activation, and blocks prostate cancer initiation caused by PTEN loss, Cancer Cell, 9, 367, 10.1016/j.ccr.2006.03.031 · DOI
- Manning, 2004, Balancing Akt with S6K: implications for both metabolic diseases and tumorigenesis, J. Cell Biol., 167, 399, 10.1083/jcb.200408161 · DOI
- Manning, 2007, AKT/PKB signaling: navigating downstream, Cell, 129, 1261, 10.1016/j.cell.2007.06.009 · DOI · Paper page
- Masri, 2007, mTORC2 activity is elevated in gliomas and promotes growth and cell motility via overexpression of rictor, Cancer Res., 67, 11712, 10.1158/0008-5472.CAN-07-2223 · DOI
- Phung, 2006, Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin, Cancer Cell, 10, 159, 10.1016/j.ccr.2006.07.003 · DOI
- Podsypanina, 1999, Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems, Proc. Natl. Acad. Sci. USA, 96, 1563, 10.1073/pnas.96.4.1563 · DOI
- Rowinsky, 2004, Targeting the molecular target of rapamycin (mTOR), Curr. Opin. Oncol., 16, 564, 10.1097/01.cco.0000143964.74936.d1 · DOI
- Salmena, 2008, Tenets of PTEN tumor suppression, Cell, 133, 403, 10.1016/j.cell.2008.04.013 · DOI
- Sarbassov, 2004, Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton, Curr. Biol., 14, 1296, 10.1016/j.cub.2004.06.054 · DOI · Paper page
- Sarbassov, 2006, Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB, Mol. Cell, 22, 159, 10.1016/j.molcel.2006.03.029 · DOI · Paper page
- Shiota, 2006, Multiallelic disruption of the rictor gene in mice reveals that mTOR complex 2 is essential for fetal growth and viability, Dev. Cell, 11, 583, 10.1016/j.devcel.2006.08.013 · DOI
- Shor, 2008, A new pharmacologic action of CCI-779 involves FKBP12-independent inhibition of mTOR kinase activity and profound repression of global protein synthesis, Cancer Res., 68, 2934, 10.1158/0008-5472.CAN-07-6487 · DOI
- Skeen, 2006, Akt deficiency impairs normal cell proliferation and suppresses oncogenesis in a p53-independent and mTORC1-dependent manner, Cancer Cell, 10, 269, 10.1016/j.ccr.2006.08.022 · DOI
- Suzuki, 1998, High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice, Curr. Biol., 8, 1169, 10.1016/S0960-9822(07)00488-5 · DOI
- Suzuki, 1998, Interfocal heterogeneity of PTEN/MMAC1 gene alterations in multiple metastatic prostate cancer tissues, Cancer Res., 58, 204
- Tessier, 2006, Serum and glucocorticoid-regulated protein kinases: variations on a theme, J. Cell. Biochem., 98, 1391, 10.1002/jcb.20894 · DOI
- Trotman, 2003, Pten dose dictates cancer progression in the prostate, PLoS Biol., 1, E59, 10.1371/journal.pbio.0000059 · DOI
- Vander Haar, 2007, Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40, Nat. Cell Biol., 9, 316, 10.1038/ncb1547 · DOI
- Vignot, 2005, mTOR-targeted therapy of cancer with rapamycin derivatives, Ann. Oncol., 16, 525, 10.1093/annonc/mdi113 · DOI
- Wang, 2003, Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer, Cancer Cell, 4, 209, 10.1016/S1535-6108(03)00215-0 · DOI · Paper page
- Wu, 2001, Generation of a prostate epithelial cell-specific Cre transgenic mouse model for tissue-specific gene ablation, Mech. Dev., 101, 61, 10.1016/S0925-4773(00)00551-7 · DOI
- Yang, 2006, Identification of Sin1 as an essential TORC2 component required for complex formation and kinase activity, Genes Dev., 20, 2820, 10.1101/gad.1461206 · DOI
- Zeng, 2006, Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML, Blood, 109, 3509, 10.1182/blood-2006-06-030833 · DOI
Cited by
Sorted by citations
mTOR Signaling in Growth, Metabolism, and Disease
Saxton, R. A., & Sabatini, D. M. (2017) · Cell · doi:10.1016/j.cell.2017.02.004 · Cited by 7,555
Self-citationmTOR: from growth signal integration to cancer, diabetes and ageing
Zoncu, R., Efeyan, A., & Sabatini, D. M. (2011) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3025 · Cited by 3,941
Self-citationMTOR: a pharmacologic target for autophagy regulation
Kim, Y. C., & Guan, K.-L. (2015) · Journal of Clinical Investigation · doi:10.1172/jci73939 · Cited by 2,126
The translational landscape of mTOR signalling steers cancer initiation and metastasis
Hsieh, A. C., Liu, Y., Edlind, M. P., Ingolia, N. T., Janes, M. R., Sher, A., Shi, E. Y., Stumpf, C. R., Christensen, C., Bonham, M. J., et al. (2012) · Nature · doi:10.1038/nature10912 · Cited by 1,313
Rapamycin-Induced Insulin Resistance Is Mediated by mTORC2 Loss and Uncoupled from Longevity
Lamming, D. W., Ye, L., Katajisto, P., Goncalves, M. D., Saitoh, M., Stevens, D. M., Davis, J. G., Salmon, A. B., Richardson, A., Ahima, R. S., et al. (2012) · Science · doi:10.1126/science.1215135 · Cited by 1,199
Self-citation
Metadata
- Authors
- Guertin, D. A., Stevens, D. M., Saitoh, M., Kinkel, S., Crosby, K., Sheen, J.-H., Mullholland, D. J., Magnuson, M. A., Wu, H., & Sabatini, D. M.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 15
- Issue
- 2
- Pages
- 148-159
- ISSN
- 1535-6108
- PMC
- PMC2701381
- Cited by
- 355
- References
- 2
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2118 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Funders
- Howard Hughes Medical Institute
- W. M. Keck Foundation
- Damon Runyon Cancer Research Foundation
- Leukemia and Lymphoma Society
- National Institutes of Health (K99 CA1296613-01A1, R01 AI04389, R01 CA103866, R01 CA107166)
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