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AKT1 — TBC1D4
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Kramer et al., Diabetes 2006
:
While
Akt and AMPK alpha2 activities are
essential for
AS160 phosphorylation by insulin and AICAR, respectively, neither kinase is indispensable for the entire effects of contraction on AS160 phosphorylation
Ramm et al., J Biol Chem 2006
:
14-3-3 proteins interact with
AS160 in an insulin- and
Akt dependent manner via an Akt phosphorylation site, Thr-642
Funai et al., Diabetes 2009
:
To evaluate the
roles of AMPK and
Akt on insulin- or contraction stimulated
PAS-AS160 , PAS-TBC1D1, and glucose transport, rat epitrochlearis was incubated with and without compound C ( inhibitor of AMPK ) or Wortmannin ( inhibitor of phosphatidylinositol [ PI] 3-kinase, which is upstream of Akt ) before and during insulin stimulation or contraction ... These data suggest that 1 ) insulin stimulates glucose transport and phosphorylation of AS160 and TBC1D1 in a PI 3-kinase/Akt dependent manner, 2 ) contraction stimulates
PAS-AS160 ( but not PAS-TBC1D1 or glucose transport ) in a PI
3-kinase/Akt dependent manner, and 3 ) contraction stimulates PAS-TBC1D1 and glucose transport ( but not PAS-AS160 ) in an AMPK dependent manner