Gene interactions and pathways from curated databases and text-mining

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CDKN1B — PTEN

Pathways - manually collected, often from reviews:

  • 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
  • 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.
  • 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