ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS
By Angela Alexander, S. Cai, Jinhee Kim, A. Nañez, Mustafa Sahin, K. Maclean, K. Inoki, K. Guan, Jianjun Shen, M. Person and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2010
712 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1f0e97027aa0502c0fb4d4d9a3f81a4ffa25f582
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In Epidemiology
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- D. Klionsky
- Nektarios Tavernarakis
- F. Cecconi
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In Molecular Biology
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Citations in the corpus
- Signal transduction by reactive oxygen species (2011, background): “, 2007), altering mTOR-dependent autophagy (Alexander et al., 2010) or modulating the synthesis of NADPH through the pentose phosphate shunt (Cosentino et al.”
- Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “tumour suppressor to inhibit mTORC1 and induce autophagy (Figure 4).(126) These new findings integrate different stress response pathways occurring in different cellular compartments.”
- AMPK - a nutrient and energy sensor that maintains energy homeostasis (2012, neutral): “It has also been suggested that H 2 O 2 can activate AMPK via a third mechanism involving a cytoplasmic form of the phosphoinositide 3-kinase-like kinase (PIKK) ataxia telangiectasia mutated (ATM”
- Oxidative stress, inflammation, and cancer: how are they linked? (2010, neutral): “ATM [101]”
- Crosstalk between apoptosis, necrosis and autophagy. (2013, methodology): “PARP1activationinresponsetoDNAdam-age can lead sequentially to ATP depletion, AMPK activation, inhibition of mTOR and autophagy induction [139 – 141].”
- Translational regulation of gene expression during conditions of cell stress. (2010, background): “Recently, an additional pathway has been indentified in which ATM directly activates LKB1/AMPK leading to a decrease in mTOR activity through TSC2, independently of p53 (Alexander et al., 2010).”
- Autophagy and the integrated stress response (2010, neutral): “, 2008) or indirectly, via activation of PARP1 (as a result of DNA damage) and/or via activation of a cytoplasmic pool of ATM and the subsequent activation of LKB1 and AMPK1 (Alexander et al., 2010; Huang et al., 2009).”
- The Role of Autophagy in Cancer: Therapeutic Implications (2011, background): “Colorectal cancer In vitro, in vivo CQ þ bortezomib (63) CQ þ vorinostat (56) Phase II HCQ þ XELOX þ bevacizumab Gastrointestinal stromal tumor In vitro, in vivo CQ þ imatinib (75) Prostate cancer In vitro, in vivo CQ þ Src kinase inhibitors (57) Vulvar cancer In vitro CQ þ cetuximab (34) Chronic my”
- Co-occurring genomic alterations define major subsets of KRAS - mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities (2015, neutral): “Activation of LKB1 through ATM-dependent phosphorylation at Thr366 in response to genotoxic or oxidative stress has been recently reported and may account for this predilection (43).”
- The regulation of autophagy – unanswered questions (2011, background): “This raises the question whether AMPK is a downstream target of TORC1 in mammals, and Snf1 an upstream effector of TORC1 in yeast?”