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AKT1 — AKT1S1

Pathways - manually collected, often from reviews:

• NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met): mTORC1/PRAS40/DEPTOR complex (MTOR-MLST8-AKT1S1-DEPTOR-RPTOR) → AKT1-2-active (AKT1/AKT2) (modification, collaborate) Takeuchi et al., J Biol Chem 2001, Moumen et al., Development 2007
  Evidence: mutant phenotype
• NCI Pathway Database mTOR signaling pathway: AKT1 (AKT1) → mTORC1/PRAS40/DEPTOR complex (MTOR-MLST8-AKT1S1-DEPTOR-RPTOR) (modification, activates)
  Garami et al., Mol Cell 2003, Inoki et al., Genes Dev 2003, Vander Haar et al., Nat Cell Biol 2007, Sancak et al., Mol Cell 2007, Wang et al., J Biol Chem 2007, Peterson et al., Cell 2009
  Evidence: mutant phenotype, assay, physical interaction
• NCI Pathway Database mTOR signaling pathway: AKT1 (AKT1) → PRAS40 (AKT1S1) (modification, activates) Garami et al., Mol Cell 2003, Inoki et al., Genes Dev 2003, Vander Haar et al., Nat Cell Biol 2007, Sancak et al., Mol Cell 2007, Wang et al., J Biol Chem 2007, Peterson et al., Cell 2009
  Evidence: mutant phenotype, assay, physical interaction
• Reactome Reaction: AKT1 → AKT1S1 (reaction) Kovacina et al., J Biol Chem 2003*
• WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: AKT1/AKT3/AKT2 → AKT1S1 (inhibition)
• WikiPathways Target Of Rapamycin (TOR) Signaling: AKT1 → AKT1S1 (inhibition)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: AKT1 — AKT1S1 (in vitro) Kovacina et al., J Biol Chem 2003*, Saito et al., J Neurosci 2004*
• IRef Hprd Interaction: AKT1 — AKT1S1 (in vivo) Kovacina et al., J Biol Chem 2003*, Saito et al., J Neurosci 2004*
• IRef Innatedb Interaction: AKT1 — AKT1S1 (unknown, -) Kovacina et al., J Biol Chem 2003*

Text-mined interactions from Literome

Timmerman et al., J Clin Endocrinol Metab 2010 : During insulin infusion, blood flow and capillary recruitment increased in the control ( P < 0.05 ) group only ; Akt phosphorylation and glucose uptake increased in both groups ( P < 0.05 ), with no group differences ; and mTORC1 signaling increased more in control ( P < 0.05 ) than in L-NMMA
Lee et al., PloS one 2010 (Endotoxemia) : Furthermore, in vitro cellular studies demonstrated that LPS ( lipopolysaccharide ) activation of mTORC1-S6K still occurs in the presence of PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Magri et al., Cell stem cell 2011 (Epilepsy...) : Notably, mTORC1 dependent Akt inhibition and STAT3 activation were involved in the reduced self-renewal and earlier neuronal and astroglial differentiation of mutant NSCs
Willems et al., Leukemia 2012 (Leukemia, Myeloid, Acute) : In addition, the mTORC1 dependent PI3K/Akt feedback activation was fully abrogated in AZD8055 treated AML cells
Urbanska et al., J Biol Chem 2012 : We also identified Akt as a downstream effector of mTORC2 needed for proper dendritic arbor morphology, the action of which required mTORC1 and p70S6K1