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AKT1 — TBC1D1
Text-mined interactions from Literome
Chavez et al., J Biol Chem 2008
:
These results indicate that endogenous Tbc1d1 does not participate in insulin regulated GLUT4 translocation in adipocytes and suggest that the GAP activity of
Tbc1d1 is not
suppressed by
Akt phosphorylation
Taylor et al., J Biol Chem 2008
:
Purified Akt and AMPK phosphorylated
TBC1D1 in vitro, and AMPK, but not
Akt ,
reduced TBC1D1 electrophoretic mobility
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
Vichaiwong et al., Biochem J 2010
:
AMPK and
Akt regulate
TBC1D1 phosphorylation, but there must be additional upstream kinases that mediate TBC1D1 phosphorylation in skeletal muscle