The TSC-mTOR signaling pathway regulates the innate inflammatory response.
By T. Weichhart, G. Costantino, M. Poglitsch, M. Rosner, M. Zeyda, K. Stuhlmeier, T. Kolbe, T. Stulnig, W. Hörl, M. Hengstschläger and 2 more. Immunity, 2008
809 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6e2a0522f281a7646375dc6e49a56d1912fe5659
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In Immunology
In Molecular Biology
- M. Laplante
- David M. Sabatini
- S. Gordon
- A. Mantovani
- A. Sica
- Subhra K. Biswas
- G. Raimondi
- A. Thomson
Citations in the corpus
- Macrophage activation and polarization: nomenclature and experimental guidelines (2014, positive): “However, using the principles described here for systematic investigation of mTOR pathway mutants will most likely resolve why rapamycin-treated macrophages and macrophages from Raptor, Rictor, and TSC1 mutants have diverse phenotypes (Ai et al., 2014; Byles et al., 2013; Festuccia et al., 2014; Wei”
- Immunoregulatory Functions of mTOR Inhibition (2009, background): “Similarly, rapamycin increased IL-12 production and decreased IL-10 production by human DCs stimulated with LPS or Staphylococcus aureus”
- Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript CRP C Reactive Protein CSF Cerebrospinal Fluid DA Dopamine DEX Dexamethasone DST Dexamethasone Suppression Test GR Glucocorticoid Receptor 5-HIAA 5-hydroxyindoleacetic acid HPA Hypothalamic-Pituitary-Adrenal Axis IDO”
- Akt Signaling Pathway in Macrophage Activation and M1/M2 Polarization (2017, background): “In an independent study in human macrophages, TSC2 deletion decreased the M1 inflammatory response in an mTOR-dependent manner (61).”
- Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “J o u rn a l o f C e ll S c ie n c e Similarly, loss of TSC1 or TSC2, which strongly activates mTORC1, was in many studies linked to the elevation of STAT3 phosphorylation (Goncharova et al., 2009; Ma et al., 2010; Onda et al., 2002; Weichhart et al., 2008).”