◀ Back to PTEN
CDKN1B — PTEN
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
CDKN1B
→
PTEN
(increases, CDKN1B Activity)
Mamillapalli et al., Curr Biol 2001*
Evidence: We have shown previously that PTEN negatively controls the G1/S cell cycle transition and regulates the levels of p27(KIP1), a CDK inhibitor
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OpenBEL Selventa BEL large corpus:
CDKN1B
→
PTEN
(increases, CDKN1B Activity)
Weng et al., Hum Mol Genet 2001*
Evidence: Here, we demonstrate that over-expression of wild-type PTEN leads to the suppression of cell growth through the blockade of cell cycle progression, an increase in the abundance of p27, a decrease in the protein levels of cyclin D1 and the inhibition of Akt phosphorylation.
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OpenBEL Selventa BEL large corpus:
CDKN1B
→
PTEN
(increases, CDKN1B Activity)
Fujita et al., J Biol Chem 2002*
Evidence: Inhibition of serine/threonine kinase Akt signaling by some pharmacological agents or by PTEN induces G(1) arrest, in part by up-regulating p27(Kip1)
Text-mined interactions from Literome
Dreher et al., Virchows Arch 2004
(Adenocarcinoma...) :
PTEN negatively influences cell growth and
induces apoptosis, while
p27kip1 binds to cyclin-E-Cdk2 and counteracts mitosis
Jonason et al., Cell cycle (Georgetown, Tex.) 2007
:
Our previous studies showed that
PTEN expression
causes accumulation of
cyclin dependent kinase inhibitor p27 ( Kip1 ) and G ( 1 ) cell cycle arrest
Wang et al., Cancer Res 2007
:
Moreover, we showed that overexpression of
PTEN or treatment with NaBT
increased expression of the
cyclin dependent kinase inhibitor p27 ( kip1 ) in HT29 cells ; this induction was attenuated by inhibition of PTEN or JNK expression or overexpression of p65