In brief

By Vittoria Zinzalla, Daniele Stracka, W. Oppliger, Michael N. Hall. Nature reviews. Molecular cell biology, 2011

625 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/5333599f3af3405ba4028df768495bc99013b314

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. David M. Sabatini
2. M. Laplante
3. Michael N. Hall
4. R. A. Saxton
5. K. Guan
6. Young Chul Kim
7. R. Loewith
8. Mustafa Sahin

Citations in the corpus

• Glutaminolysis activates Rag-mTORC1 signaling. (2012, background): “The two best characterized substrates of mTORC1 are S6K and 4EBP1. mTORC2 comprises mTOR, Rictor, mSIN1, PRR5, and Mo mLST8 and phosphorylates several AGC kinases, such as AKT and SGK1, in response to growth factors (Cybulski and Hall, 2009; Zinzalla et al., 2011).”
• The Neurology of mTOR (2014, positive): “In yeast and cancer cells, mTORC2 associates with the ribosome, which appears to be crucial to mTORC2 activation (Zinzalla et al., 2011).”
• mTOR signaling in growth control and disease (2012, positive): “One potential mechanism involves a new role for ribosomes, as ribosomes are needed for mTORC2 activation and mTORC2 binds them in a PI3K-dependent fashion (Zinzalla et al., 2011).”
• Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, background): “The ribosome has recently been shown to be a necessary factor for mTORC2 activit”
• mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “Another study found that PI3K promotes the association of mTORC2 with ribosomes to activate its kinase activity, although the mechanistic basis for this is unclear (Zinzalla et al., 2011).”
• Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “So far, only PI3K stimulation has been shown to promote mTORC2 activation in association with the mSIN1 PH domain and the ribosome (Liu et al., 2015; Zinzalla et al., 2011).”
• TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “C interaction with the ribosome activate TORC2, which in turn activates AKT, SGK, and related kinases (Oh et al., 2010; Zinzalla et al., 2011; Zoncu et al., 2011).”
• Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “lysosomes in a PI3K-dependent fashion (Zinzalla et al., 2011).”
• Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control (2011, background): “Zinzalla et al. (2011) recently devised a “reverse” suppressor screen to identify upstream regulators of TORC2.”
• mTOR: a pharmacologic target for autophagy regulation. (2015, positive): “However, it was proposed that insulin/PI3K signaling activates mTORC2 by promoting its interaction with ribosome, and subsequently mTORC2 phosphorylates AKT at the turn motif site, Thr450, during translation (48, 80).”
• mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “Another study found that PI3K promotes the association of mTORC2 with ribosomes to activate its kinase activity, although themechanistic basis for this is unclear (Zinzalla et al., 2011).”