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AKT3 — PRKCZ
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
AKT3
—
PRKCZ
(direct interaction, two hybrid)
Hodgkinson et al., Biochemistry 2002*
-
IRef Biogrid Interaction:
AKT3
—
PRKCZ
(physical association, affinity chromatography technology)
Hodgkinson et al., Biochemistry 2002*
-
IRef Biogrid Interaction:
AKT3
—
PRKCZ
(direct interaction, enzymatic study)
Hodgkinson et al., Biochemistry 2002*
-
IRef Hprd Interaction:
AKT3
—
PRKCZ
(in vitro)
Hodgkinson et al., Biochemistry 2002*, Li et al., J Biol Chem 1997*, Walker et al., Biochem J 1998*
-
IRef Hprd Interaction:
AKT3
—
PRKCZ
(in vivo)
Hodgkinson et al., Biochemistry 2002*, Li et al., J Biol Chem 1997*, Walker et al., Biochem J 1998*
-
IRef Innatedb Interaction:
PRKCZ
—
AKT3
(unknown, -)
Hodgkinson et al., Biochemistry 2002*
-
IRef Ophid Interaction:
PRKCZ
—
AKT3
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
STRING interaction:
AKT3
—
PRKCZ
(interaction, mapped from kegg_pathways)
-
STRING interaction:
AKT3
—
PRKCZ
(interaction, mapped from kegg_pathways)
-
STRING interaction:
PRKCZ
—
AKT3
(interaction, mapped from kegg_pathways)
-
STRING interaction:
PRKCZ
—
AKT3
(interaction, mapped from kegg_pathways)
Text-mined interactions from Literome
Martelli et al., Leukemia 2003
:
At variance with Ly294002, the
Akt inhibitor did not negatively
affect phosphorylation of
protein kinase C-zeta and it was less effective in downregulating p70S6 kinase (p70S6K) activity
Brubaker et al., Endocrinology 2004
:
The proliferative effects of GLP-1 appear to involve multiple intracellular pathways, including stimulation of
Akt ,
activation of
protein kinase Czeta , and transactivation of the epidermal growth factor receptor through the c-src kinase
Corbould et al., J Endocrinol 2007
(Insulin Resistance...) :
In the glucose metabolic pathway of insulin signaling, treatment of cells with T 10 nmol/l did not alter insulin stimulated phosphorylation of insulin receptor substrate-1 or
Akt , but insulin stimulated phosphorylation of
protein kinase C (PKC) zeta was
impaired