IGF1R

(redirected from IGF-I receptor)

IGF1R

A gene on chromosome 15q26.3 that encodes a tyrosine kinase receptor with a high binding affinity for insulin-like growth factor, which plays a key role in transformation events in cell growth and survival.

Molecular pathology
IGF1R is highly overexpressed in cancer where it has anti-apoptotic activity, enhancing malignant cell survival.
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Moreover, using semiquantitative polymerase chain reaction (PCR), Tittle et al [7] showed that IGF-I receptor mRNA was downregulated in rat HFs upon the onset of the catagen stage.
The upregulation of IRS-4 levels induced the activation of the IGF-I receptor pathway and increased the phosphorylation of AKT, mTOR, p70S6 kinase, GSK-3 and ERK in both cell types (Figure 1(c)).
Primary GH insensitivity is caused by genetic disorders involving GHR or its downstream mediators such as STAT5b, the IGFI/IGFBP3-stabilized acid labile subunit (ALS), IGF-I, or the IGF-I receptor gene [21].
Valentinis, "The IGF-I receptor in cell growth, transformation and apoptosis," Biochimica et Biophysica Acta (BBA)--Reviews on Cancer, vol.
IGF-I receptor (IGF-IR) belongs, along with the IR, to the class II receptor tyrosine kinase superfamily.
The IGF-I receptor can alter the matrix metalloproteinase repertoire of tumor cells through transcriptional regulation of PKC-{alpha}.
It mediates its effects through the IGF-I receptor (IGF-IR) that belongs to the tyrosine kinase family of growth factor receptors [9].
Effects of aging and caloric restriction on IGF-I, IGF-I receptor, IGFBP-3 and IGFBP-4 gene expression in the rat stomach and colon.
Interestingly, SOCS2 was first cloned using a yeast two-hybrid system with the IGF-I receptor as a bait [70].
Unlike most of the other binding proteins, which act as competitive inhibitors of IGF-I receptor, IGFBP-5 acts to enhance IGF-I actions.
Benini et al., "Expression of an IGF-I receptor dominant negative mutant induces apoptosis, inhibits tumorigenesis and enhances chemosensitivity in Ewing's sarcoma cells," International Journal of Cancer, vol.