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Review
. 2017 Feb 15;36(4):397-408.
doi: 10.15252/embj.201696010. Epub 2017 Jan 17.

Nutrient sensing and TOR signaling in yeast and mammals

Affiliations
Review

Nutrient sensing and TOR signaling in yeast and mammals

Asier González et al. EMBO J. .

Abstract

Coordinating cell growth with nutrient availability is critical for cell survival. The evolutionarily conserved TOR (target of rapamycin) controls cell growth in response to nutrients, in particular amino acids. As a central controller of cell growth, mTOR (mammalian TOR) is implicated in several disorders, including cancer, obesity, and diabetes. Here, we review how nutrient availability is sensed and transduced to TOR in budding yeast and mammals. A better understanding of how nutrient availability is transduced to TOR may allow novel strategies in the treatment for mTOR-related diseases.

Keywords: RAG; TORC1; amino acids; glucose; mammals; nutrients; yeast.

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Figures

Figure 1
Figure 1. Regulation of TORC1 by amino acids in yeast (Saccharomyces cerevisiae) and mammals
Proteins shown in green promote TORC1 activation. Proteins in red inhibit TORC1. GAP and GEF between parentheses indicate that the proteins act as GTPase‐activating proteins or guanine exchange factors, respectively. Dashed lines indicate indirect interactions. There is no evidence that the yeast RHEB‐related protein Rhb1 plays a role in TORC1 regulation. See main text for details.
Figure 2
Figure 2. Crosstalk between TORC1 and GAAC signaling pathways in yeast and mammals
Proteins shown in green promote Gcn4/ATF4‐dependent transcription. Proteins in red inhibit Gcn4/ATF4‐dependent transcription. PPase, protein phosphatase. See main text for details.
Figure 3
Figure 3. Crosstalk between TORC1 and AMPK signaling pathways in yeast and mammals
Proteins shown in green promote TORC1 activation. Proteins in red inhibit TORC1. IRS1, insulin receptor substrate 1. See main text for details.

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