Gene interactions and pathways from curated databases and text-mining

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AKT1 — APPL1

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Lin et al., Mol Cell Biol 2006 : Reduction of APPL1 or GIPC1 protein levels suppressed nerve growth factor (NGF) dependent MEK, extracellular signal regulated kinase, and Akt activation and neurite outgrowth in PC12 cells
Saito et al., J Biol Chem 2007 : We show that APPL1 knockdown suppressed Akt phosphorylation, glucose uptake, and Glut4 translocation
Schenck et al., Cell 2008 : We show that in zebrafish, Appl1 regulates Akt activity and substrate specificity, controlling GSK-3beta but not TSC2
Cheng et al., Cell Metab 2009 (Diabetes Mellitus, Type 2) : Insulin stimulated activation of Akt and suppression of gluconeogenesis in hepatocytes are enhanced by APPL1 overexpression, but are attenuated by APPL1 knockdown ... APPL1 interacts with Akt and blocks the association of Akt with its endogenous inhibitor tribble 3 (TRB3) through direct competition, thereby promoting Akt translocation to the plasma membrane and the endosomes for further activation
Bae et al., Mol Biol Cell 2010 : Both Cdo and APPL1 are required for efficient Akt activation during myoblast differentiation
Tu et al., J Biol Chem 2011 (Bone Resorption) : Adiponectin inhibits osteoclastogenesis and bone resorption via APPL1 mediated suppression of Akt1 ... Using siRNA specifically targeting APPL1, the first identified adaptor protein of adiponectin signaling, we found that the inhibitory effect of adiponectin on osteoclasts was induced by APPL1 mediated down-regulation of Akt1 activity
Wang et al., Diabetes 2011 (Insulin Resistance...) : In endothelial cells, APPL1 potentiated insulin stimulated Akt activation by competing with the Akt inhibitor Tribbles 3 (TRB3) and suppressed ERK1/2 signaling by altering the phosphorylation status of its upstream kinase Raf-1 ... In endothelial cells, APPL1 potentiated insulin stimulated Akt activation by competing with the Akt inhibitor Tribbles 3 (TRB3) and suppressed ERK1/2 signaling by altering the phosphorylation status of its upstream kinase Raf-1