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AKT1 — PTPN1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B (PTPN1)
→
PTP1B/AKT1 complex (PTPN1-AKT1)
(modification, collaborate)
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B (PTPN1)
→
AKT1 (AKT1)
(modification, collaborate)
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B/AKT1 complex (PTPN1-AKT1)
→
AKT1 (AKT1)
(modification, collaborate)
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B (PTPN1)
→
PTP1B/AKT1 complex (PTPN1-AKT1)
(modification, activates)
Elchebly et al., Science 1999*, Ravichandran et al., Mol Endocrinol 2001
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B/AKT1 complex (PTPN1-AKT1)
→
Insulin Receptor/Insulin complex (INSR-INS)
(modification, inhibits)
Elchebly et al., Science 1999*, Ravichandran et al., Mol Endocrinol 2001
Evidence: mutant phenotype, assay, physical interaction, other species
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Egawa et al., J Biol Chem 2001
(Carcinoma, Hepatocellular...) :
These effects were specific for insulin signaling, because platelet derived growth factor ( PDGF ) -stimulated PDGF receptor tyrosine phosphorylation and
Akt phosphorylation were not
inhibited by
PTP1B overexpression ... In both cells,
PTP1B overexpression blocked insulin stimulated tyrosine phosphorylation of the insulin receptor and IRS-1 by more than 70 % and
resulted in a significant inhibition of the association between IRS-1 and the p85 subunit of phosphatidylinositol 3-kinase and
Akt phosphorylation as well as mitogen activated protein kinase phosphorylation
Shimizu et al., Endocrinology 2002
:
Mechanism for differential
effect of
protein-tyrosine phosphatase 1B on
Akt versus mitogen activated protein kinase in 3T3-L1 adipocytes
Clampit et al., Biochem Biophys Res Commun 2003
(Carcinoma, Hepatocellular) :
Reduction of
PTP1B expression in FAO cells also
caused an increase in insulin stimulated phosphorylation of
PKB and GSK3, without any change in protein expression
Vercauteren et al., Circulation 2006
(Cardiac Output, Low) :
PTP1B inhibition stimulated early eNOS phosphorylation and
increased phosphorylation of
Akt
Venkatesan et al., FASEB J 2008
:
Interestingly, resveratrol
increased the activity of protein tyrosine phosphatase
PTP1B , which dephosphorylates PDGF stimulated phosphorylation at tyrosine-751 and tyrosine-716 on PDGFR with concomitant reduction in
Akt and Erk1/2 kinase activity
González-RodrĂguez et al., Diabetes 2010
:
The absence of
PTP1B in the double-mutant mice
restored hepatic IRS1 mediated phosphatidylinositol (PI)
3-kinase/Akt/Foxo1 signaling
Chen et al., Biochem Biophys Res Commun 2010
(Hyperglycemia...) :
Here we report that BBR mimics insulin action by increasing glucose uptake ability by 3T3-L1 adipocytes and L6 myocytes in an insulin independent manner,
inhibiting phosphatase activity of
protein tyrosine phosphatase 1B (PTP1B) , and increasing phosphorylation of IR, IRS1 and
Akt in 3T3-L1 adipocytes
Wang et al., Med Oncol 2012
(Disease Progression...) :
Overexpression of
PTP1B promoted the proliferation and in vivo tumorigenesis of MKN45 cells and also
increased the phosphorylation levels of
Akt , Erk1/2, and FAK and the activity of Src
Stull et al., Diabetes 2012
(Diabetes Mellitus, Type 2...) :
PTP1B overexpression
resulted in reduction of
Akt phosphorylation in the control subjects