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IGF1R — TP53
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
IGF1R
→
TP53
(decreases)
Evidence: pIGF-IR (Tyr1131), pIGF-IR (Tyr1135/1136; data not shown), and pAkt (Ser473) levels were obviously higher in HBEC cells expressing p53i and/or RASv12 than in parental HBEC cells (Fig. 2A, right)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Merkle et al., Gene Ther 1998
:
Neither wild-type
p53 nor p53 delta 326
repressed the transcription of the
IGF-1R gene in these cell lines
Girnita et al., Proc Natl Acad Sci U S A 2003
(Melanoma) :
One of the challenging questions remaining to be answered is why the wild-type
p53 , which per se represses the transcription of the IGF-1R gene, in overexpressed form is
necessary for a high
IGF-1R expression
Attias et al., Endocr Relat Cancer 2006
(Colonic Neoplasms) :
Folic acid and its metabolites modulate
IGF-I receptor gene expression in colon cancer cells in a
p53 dependent manner
Kavurma et al., Biochem J 2007
(Carotid Stenosis) :
Oxidative stress repressed
IGF1R expression at multiple levels, and this was also
blocked by mutant
p53 ... These results suggest that oxidative-stress induced repression of
IGF1R is
mediated by the association of phosphorylated
p53 with the IGF1R promoter via TBP, and by the subsequent recruitment of chromatin modifying proteins, such as HDAC1, to the IGF1R promoter-TBP-p53 complex
Werner et al., Proc Natl Acad Sci U S A 1996
:
Wild-type and mutant
p53 differentially
regulate transcription of the
insulin-like growth factor I receptor gene
Ohlsson et al., Endocrinology 1998
(Osteosarcoma) :
p53 regulates insulin-like growth factor-I
(IGF-I) receptor expression and IGF-I induced tyrosine phosphorylation in an osteosarcoma cell line : interaction between p53 and Sp1 ... These data indicate that the
IGF-I receptor is a physiological
target for
p53 in osteosarcoma cells