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Literature summary for 5.2.1.8 extracted from

  • Kim, M.R.; Choi, H.S.; Heo, T.H.; Hwang, S.W.; Kang, K.W.
    Induction of vascular endothelial growth factor by peptidyl-prolyl isomerase Pin1 in breast cancer cells (2008), Biochem. Biophys. Res. Commun., 369, 547-553.
    View publication on PubMed

Application

Application Comment Organism
medicine Pin1 overexpression increases the reporter activities in cells transfected with reporters containing the vascular endothelial growth factor VEGF gene promoter or with minimal reporters of activator protein-1 and hypoxia response element. VEGF reporter gene activity is significantly inhibited by either hypoxia-inducible factor-alpha siRNA or AP-1 decoy ODN. Pin1 stimulates VEGF expression by activating HIF-1alpha and AP-1, and is a potential therapeutic target of angiogenesis during cancer development Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information Pin1 overexpression increases the reporter activities in cells transfected with reporters containing the vascular endothelial growth factor VEGF gene promoter or with minimal reporters of activator protein-1 and hypoxia response element. VEGF reporter gene activity is significantly inhibited by either hypoxia-inducible factor-alpha siRNA or AP-1 decoy ODN. Pin1 stimulates VEGF expression by activating HIF-1alpha and AP-1, and is a potential therapeutic target of angiogenesis during cancer development Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
isoform Pin1
-