Gene interactions and pathways from curated databases and text-mining

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IGFBP3 — TP53

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: IGFBP3 → TP53 (increases)
    Evidence: IGFBP-3 production has been shown to be increased by cell growth-inhibitory agents, such as transforming growth factor-beta (TGF-beta), and the tumor suppressor gene p53.
  • OpenBEL Selventa BEL large corpus: IGFBP3 → TP53 (increases)
    Evidence: Supporting its role as a primary growth inhibitor, IGFBP-3 production has been shown to be increased by cell growth-inhibitory agents, such as transforming growth factor-beta (TGF-beta), and the tumor suppressor gene p53.
  • BioCarta hypoxia and p53 in the cardiovascular system: TFIID/RPA/JNK/p300/p53 complex (TAF1-RPA1-MAPK8-EP300-TP53) → IGFBP3 (transcription, activates)
  • KEGG p53 signaling pathway: TP53 → IGFBP3 (gene expression, expression)
  • KEGG p53 signaling pathway: TP53 → IGFBP3 (gene expression, expression)

Text-mined interactions from Literome

Hanafusa et al., BMC cancer 2005 (Carcinoma, Hepatocellular...) : Deletions and mutations of these sequences completely abolished the expression of IGFBP-3 in the presence of p53 overexpression
Harms et al., Mol Cell Biol 2005 : We found that the IGFBP3 promoter was activated by p53 ( DeltaNDeltaBD ), which mimics a naturally occurring N- and C-terminally truncated human p53 isoform, and by p53AS, a C-terminally truncated murine p53 isoform generated through alternative splicing, but not by full-length human or murine p53 ... In addition, we identified that histone deacetylase activity, not p53 DNA binding ability, governs the regulation of IGFBP3 by full-length p53 family proteins, as inhibition of histone deacetylases restores the induction of IGFBP3 by exogenous full-length p53 , p63, and p73 proteins ... Furthermore, we found that activation of p53 or inhibition of histone deacetylases alone was not sufficient to induce IGFBP3 ; however, combined treatment endowed endogenous p53 with this activity
Grimberg et al., J Clin Endocrinol Metab 2005 (Lung Neoplasms) : Induction of IGFBP-3 by the tumor suppressor p53 has been shown in various models that directly manipulate p53 activity ... Finally, we have established that IGFBP-3 induction under hypoxic conditions is independent of p53 in tumor cell lines derived form multiple tissue types
Mochizuki et al., Growth Horm IGF Res 2006 (Endometrial Neoplasms) : IGFBP-3 inhibited BrdU uptake, potentiated ssDNA production and induced p53 in HHUA cells
Ho et al., Cancer Cell 2009 (Bone Neoplasms...) : Regulation of Igfbp3 expression and insulin-like growth factor (IGF) signaling by Gli and p53 integrated their effect on apoptosis
Wang et al., Invest Ophthalmol Vis Sci 2013 : How overexpression of SIRT1 promotes HG-attenuated corneal epithelial wound healing via p53 regulation of the IGFBP3 ( insulin-like growth factor binding protein-3 ) /IGF-1 ( insulin-like growth factor-1 ) /AKT pathway was investigated in CECs and Ins2 ( Akita/+ ) mice
Buckbinder et al., Nature 1995 : Induction of the growth inhibitor IGF binding protein 3 by p53 ... Induction of IGF-BP3 gene expression by wild-type but not mutant p53 is associated with enhanced secretion of an active form of IGF-BP3 capable of inhibiting mitogenic signalling by the insulin-like growth factor IGF-1