Glutaminolysis activates Rag-mTORC1 signaling.
By Raúl V. Dúran, W. Oppliger, Aaron M. Robitaille, L. Heiserich, Roswitha Skendaj, Eyal Gottlieb, Michael N. Hall. Molecules and Cells, 2012
689 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/34f0c28bb3bddfa2aa9c7bb859bda789561f2b45
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Citations in the corpus
- Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “Furthermore, glutaminolysis can promote the loading of the mTOR translocation recruiter RagB GTP because glutamine promotes the conversion of GDP (guanosine diphosphate) to GTP (guanosine triphosphate) (99).”
- From Krebs to Clinic: Glutamine Metabolism to Cancer Therapy (2016, background): “BPTES inhibition of hGA(124-551), a truncated form of human kidneytype glutaminase.”
- Targeting cellular metabolism to improve cancer therapeutics (2013, background): “Glutaminolysis activates mTORC1 signaling and inhibition of glutaminolysis via GLS inhibitors (DON and BPTES) or siRNAtargeting GLS or GDH, prevents mTORC1 activation.(97) It is”
- Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “α-ketoglutarate generated upon double deamination occurring in the glutaminolytic pathway.(26) Although mTOR activation through this mechanism needs to be still clarified, it seems to”
- Inflammatory T cell responses rely on amino acid transporter ASCT2 facilitation of glutamine uptake and mTORC1 kinase activation (2014, neutral): “, 2010) and that glutamine and leucine might cooperate in this pathway of mTORC1 activation (Durán et al., 2012).”
- Nutrient sensing and TOR signaling in yeast and mammals (2017, neutral): “GDH (glutamate dehydrogenase), which requires leucine as a cofactor, then converts glutamate to a -ketoglutarate. a -Ketoglutarate activates RAG-mTORC1 through PHD (prolyl hydroxylase) (Dura´n et al , 2012, 2013).”