Dysregulation of the TSC-mTOR pathway in human disease

By K. Inoki, M. Corradetti, K. Guan. Nature Genetics, 2004

1,008 citations recorded by the source corpus.

Subfields: Management, Monitoring, Policy and Law, Political Science and International Relations

View Paper: https://www.semanticscholar.org/paper/618bff919b287e6160031bb5537d85d8d00b7379

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Citations in the corpus

The plasticity of aging: insights from long-lived mutants. (2005, neutral): “In addition, PTEN mutations activate the growth-promoting TOR pathway, and this appears to promote certain types of cancer as well (Inoki et al., 2005).”
Fuel feeds function: energy metabolism and the T-cell response (2005, neutral): “For in-depth discussion, see several recent review”
TOR signaling in growth and metabolism. (2006, background): “Specifically, aberrantly high mTORC1 activity appears to be an underlying cause of cancers and hamartoma syndromes (Inoki et al., 2005; Tee and Blenis, 2005).”
ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010, background): “TSC2 participates in energy sensing and growth factor signaling to repress the kinase mTOR in the mTORC1 complex, a key regulator of protein synthesis and cell growth (7, 8).”
Regulation of cancer cell metabolism (2011, background): “In addition to its stabilization under hypoxic conditions, HIF1 can also be activated under normoxic conditions by oncogenic signalling pathways, including PI3”
Succinate dehydrogenase and fumarate hydratase: linking mitochondrial dysfunction and cancer (2006, background): “The mTOR-dependent translation of HIFa is induced by the loss of the Tsc1, Tsc2 or Lkb1 tumour suppressor genes and potentially by activation via the Akt pathway (Inoki et al., 2005; Plas and Thompson, 2005).”
A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, positive): “As mTOR plays a critical role in controlling cell growth (Aoki and Vogt, 2004; Inoki et al., 2005), these biochemical data raised the possibility that cooperative inhibition of p110 a and mTOR may underlie the efﬁcacy of PI-103 in glioma cells.”