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EGR1 — PTEN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Virolle et al., Nat Cell Biol 2001
(Neoplasms) :
Therefore,
Egr-1 can directly
regulate PTEN , triggering the initial step in this apoptotic pathway
Moorehead et al., J Biol Chem 2003
:
IGF-II induced
PTEN promoter activity and protein levels and this
involved the immediate early gene
egr-1
Tell et al., Endocrinology 2004
(Thyroid Neoplasms) :
Cotransfection experiments indicated that in normal FRTL-5 rat thyroid cells,
PTEN promoter activity was
increased by overexpression of the transcription factor
early growth response protein-1 (Egr-1)
Okamura et al., J Cell Biochem 2005
:
These observations also support the view that
EGR-1 regulates
PTEN expression in the initial steps of the apoptotic pathway
Kim et al., Cancer Res 2006
:
These results show that survival signals generated by PLD attenuate expression of Egr-1 by activation of phosphatidylinositol 3-kinase signaling pathway and
induction of
PTEN by
Egr-1 , which confers resistance to apoptosis
Fernández et al., Biochim Biophys Acta 2008
:
Inhibition of PTEN involved activation of a PI3K/protein kinase C ( PKC ) pathway that decreased in a proteasome dependent step the levels of the transcription factor
Egr-1 , a key
regulator of
PTEN levels in astrocytes, causing decreased binding of Egr-1 to the PTEN promoter
Fantini et al., Free radical research 2008
:
APE1/Ref-1 regulates
PTEN expression
mediated by
Egr-1 ... That APE1 dependent
PTEN expression is
mediated by
Egr-1 was supported by experiments with cells ectopically expressing Egr-1
Lau et al., Oncogene 2011
(Ovarian Neoplasms) :
E-cadherin inhibits tumor cell growth by suppressing PI3K/Akt signaling via
ß-catenin-Egr1 mediated
PTEN expression ... In summary, endogenous E-cadherin inhibits PI3K/Akt signaling by antagonizing
ß-catenin-Egr1 mediated repression of
PTEN expression