Gene interactions and pathways from curated databases and text-mining

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AKT1 — PAWR

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: PAWR → AKT1 (decreases, AKT1 Activity, PAWR Activity)
    Evidence: The interaction of the cell survival kinase, Akt1 (5), with the prostate apoptosis response-4 protein, Par-4 (6), results in phosphorylation and silencing of Par-4
  • OpenBEL Selventa BEL large corpus: PAWR → AKT1 (decreases, AKT1 Activity, PAWR Activity)
    Evidence: mutations in the Par-4 gene have not been reported in cancer cells. Accordingly, endogenous Par-4 must be bound and functionally inactivated by an antiapoptotic protein, which prevents Par-4 from executing its proapoptotic functions. Indeed, our recent studies reveal that binding of Akt1 to Par-4 results in both Par-4 phosphorylation and inactivation of its proapoptotic potential (7).
  • OpenBEL Selventa BEL large corpus: PAWR → AKT1 (increases, PAWR Activity)
    Evidence: The interaction of the cell survival kinase, Akt1 (5), with the prostate apoptosis response-4 protein, Par-4 (6), results in phosphorylation and silencing of Par-4
  • OpenBEL Selventa BEL large corpus: PAWR → AKT1 (increases, PAWR Activity)
    Evidence: mutations in the Par-4 gene have not been reported in cancer cells. Accordingly, endogenous Par-4 must be bound and functionally inactivated by an antiapoptotic protein, which prevents Par-4 from executing its proapoptotic functions. Indeed, our recent studies reveal that binding of Akt1 to Par-4 results in both Par-4 phosphorylation and inactivation of its proapoptotic potential (7).

Text-mined interactions from Literome

Joshi et al., EMBO J 2008 (Lung Neoplasms) : Par-4 inhibits Akt and suppresses Ras induced lung tumorigenesis ... We also demonstrate in cell culture, in vivo, and in biochemical experiments that Akt regulation by Par-4 is mediated by PKCzeta, establishing a new paradigm for Akt regulation and, likely, for Ras induced lung carcinogenesis, wherein Par-4 is a novel tumour suppressor
Diaz-Meco et al., Cell cycle (Georgetown, Tex.) 2008 (Lung Neoplasms) : Akt regulation and lung cancer : a novel role and mechanism of action for the tumor suppressor Par-4 ... We have demonstrated in cell culture, in vivo, and in biochemical experiments that Akt regulation by Par-4 is mediated by PKC zeta, establishing a new paradigm for Akt regulation and demonstrating in vivo that PKC zeta is a physiologically relevant partner of Par-4