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CALM1 — GYS1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Bode et al., Mol Cell Biochem 1988
:
Isoproterenol and prostaglandin E1 both stimulate cAMP accumulation, but only isoproterenol causes activation of particulate cAMP dependent protein kinase, leading to activation of
phosphorylase kinase and glycogen phosphorylase, and
inhibition of
glycogen synthase
Inoue et al., J Neurochem 1987
:
The results indicate that brain
glycogen synthase is regulated in a
calmodulin dependent manner similarly to the skeletal muscle enzyme, but that the brain enzyme is different from the skeletal muscle enzyme
Iwasa et al., FEBS Lett 1983
:
Ca2+,
calmodulin dependent phosphorylation of
glycogen synthase by a brain protein kinase
Picton et al., Cell Calcium 1981
:
Recent work has demonstrated that
phosphorylase kinase not only
activates phosphorylase, but also phosphorylates
glycogen synthase thereby decreasing its activity ( 45-49 )
Shashkin et al., J Biol Chem 1995
(Anoxia) :
These data demonstrate that : 1 ) hexose transport, both in the absence and presence of external stimuli ( insulin and hypoxia ), requires functional calmodulin ; and 2 ) insulin mediated activation of
glycogen synthase does not
require functional
calmodulin , nor can it be accounted for by increases in glucose transport or glucose-6-P
Sambandam et al., Microbios 1993
:
Glycogen synthase was inhibited until the 30th day by calmodulin, whereas
calmodulin obtained from the 40th day
stimulated glycogen synthase activity and the 50th day sample had no effect