◀ Back to PRKAG1
PRKAG1 — TBC1D1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Chen et al., Biochem J 2008
:
Complementary
regulation of
TBC1D1 and AS160 by growth factors, insulin and
AMPK activators
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
Pehmøller et al., Am J Physiol Endocrinol Metab 2009
:
AMPK activation by AICAR
induced similar Ser ( 237 ) and Thr ( 596 ) phosphorylation of, and 14-3-3 binding to,
TBC1D1 as muscle contraction ...
AMPK activation by AICAR
induced similar Ser ( 237 ) and Thr ( 596 ) phosphorylation of, and 14-3-3 binding to,
TBC1D1 as muscle contraction ... This study provides genetic evidence to support an important
role for
AMPK in regulating
TBC1D1 in response to both of these physiological stimuli
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