Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway.
By B. Manning, Andrew R. Tee, M. Logsdon, J. Blenis, L. C. Cantley. Molecules and Cells, 2002
1,595 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/f060372cd7c9c05c58b12cfdb817efaa651ebbfe
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In Molecular Biology
- David M. Sabatini
- M. Laplante
- K. Guan
- B. Manning
- R. A. Saxton
- Michael N. Hall
- R. Shaw
- Lewis C. Cantley
In Physiology
- David M. Sabatini
- B. Manning
- K. Guan
- M. Laplante
- Lewis C. Cantley
- R. A. Saxton
- N. Hay
- Jingxiang Huang
Citations in the corpus
- Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. (2004, background): “Akt is a serine/threonine kinase that phosphorylates many effectors including Tsc2 (Dan et al. 2002; Inoki et al. 2002; Manning et al. 2002; Potter et al. 2002).”
- mTOR regulation of autophagy (2010, background): “TSC2, in a complex with TSC1, acts as a GTPase activating protein (GAP) for the small GTPase Rheb and the GAP activity is regulated by Akt-mediated phosphorylation of TSC2 [39,40].”
- mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “In turn, Akt phosphorylates TSC2, a large protein that, together with TSC1 (also known as hamartin), forms the TSC1–TSC2 comple”
- Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “Recent work shows that hypophosphorylated TSC2 is present within the membrane fraction of cells, where it interacts with TSC1 (Cai et al., 2006).”
- Regulation of mTORC1 by amino acids (2014, neutral): “The TSC complex, whose loss underlies a hamartomatous syndrome of the same name (17, 18), serves as a central hub for numerous extracellular and intracellular inputs including mitogen and growth factor signaling (19-23), energy levels (24), oxygen availability (25, 26) and genotoxic stress (27), whi”
- Molecular mechanisms of mTOR-mediated translational control (2009, background): “A TSC2 mutant in which AKT phosphorylation sites are substituted can be a dominant inhibitor of mTORC1 by blunting its activation in response to growth factor stimul”