[10] Intriguingly, those RNAs that do not need an intron sequence to pair with could, in theory, continue to undergo editing as mature mRNA.

[10] The editing site also overlaps with an antisense transcript which could also form a double stranded RNA structure creating a suitable substrate for ADARs.

[16] At position 78 in unedited version of the transcript there is an Arginine close to residue valine-49.This Valine is important in hydrophobic interaction of Phenylalanine of IGF-1.

A substitution to a Glycine at this position is thought to introduce additional flexibility leading to a change of loop conformation, thereby disrupting the hydrophobic interaction that stabilises the complex.

[14] The edited region contains a proposed heparin binding site and is also part of the recognition sequence for proteolytic cleavage.

[17] Cleavage which occurs at amino acid position 97 reduces heparin binding but modulates the growth stimulatory activity of the protein.

Since the protein has been implicated in these processes it is believed editing might effect apoptosis, regulation of cell growth and angiogenesis.

[10] A study at the European Neuroscience Institute-Goettingen (Germany) found that fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17- to 19-day-old newborn hippocampal neurons.

This suggests that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat diseases linked to excessive fear memory such as PTSD.

These data suggest that IGFBP7 is a critical regulator of memory consolidation and might be used as biomarker for Alzheimer's disease.