Activation of a metabolic gene regulatory network downstream of mTOR complex 1.

By K. Düvel, J. Yecies, Suchithra Menon, Pichai Raman, A. Lipovsky, Amanda L. Souza, E. Triantafellow, Qicheng Ma, Regina K. Gorski, Stephen Cleaver and 6 more. Molecules and Cells, 2010

1,964 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/10c708e792bd8056862d79207fa972cbe2dfb763

How researchers see this paper

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

In Cancer Research

1. M. V. Vander Heiden
2. Ralph J. Deberardinis
3. Navdeep S. Chandel
4. David M. Sabatini
5. Craig B. Thompson
6. C. V. Dang
7. J. Cantor
8. Jie Zheng

In Molecular Biology

1. David M. Sabatini
2. M. V. Vander Heiden
3. Ralph J. Deberardinis
4. Craig B. Thompson
5. Navdeep S. Chandel
6. M. Laplante
7. B. Manning
8. Michael N. Hall

Citations in the corpus

• Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “In addition to mediating HIFs, mTOR directly upregulates the basic glycolytic processes, from glucose uptake to lactate formation (56,58,67).”
• Nrf2 redirects glucose and glutamine into anabolic pathways in metabolic reprogramming. (2012, background): “Considering that SREBP has been suggested to induce the PPP genes when mTORC1 is activated (Düvel et al., 2010), Nrf2 could indirectly activate the PPP through the Akt-mTORC1-SREBP axis in addition to its role in the direct regulation of the PPP.”
• Tumor glycolysis as a target for cancer therapy: progress and prospects (2013, background): “Such an adaptation involves mTORC1-mediated regulation of the expression of glycolytic enzymes through the activation of genes such as c-myc and HIF1-alpha [81-83].”
• Hooked on fat: the role of lipid synthesis in cancer metabolism and tumour development (2013, background): “Furthermore, SCD1, the main isoform of SCD in humans, is induced by hypoxia in clear cell renal carcinoma cells and regulates the expression of HIF2α through a positive feedback loop involving Akt (Zhang et al., 2013).”
• mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “…to glycolysis, which likely facilitates the incorporation of nutrients into new biomass. mTORC1 increases the translation of the transcription factor HIF1a (Figure 2C), which drives the expression of several glycolytic enzymes such as phospho-fructo kinase (PFK) (Düvel et al., 2010).”
• mTOR signaling in growth control and disease (2012, background): “Interestingly, the mTORC1 pathway regulates v-ATPase expression, suggesting that a feedback loop exists between mTORC1 and lysosome function (Düvel et al., 2010; Peña-Llopis et al., 2011).”