Consequences IGFBP7

1 consequences

1.1 structural
1.2 function
1.3 functions in learning , memory

consequences
structural

the edited sites found within insulin growth factor binding domain of igfbp7 , heparin binding domain.this region site proteolytic cleavage.structural analysis of edited sites determined 2 amino acids corresponded edited sites not directly involved in binding igf-1 found in regions flanking them. @ position 78 in unedited version of transcript there arginine close residue valine-49.this valine important in hydrophobic interaction of phenylalanine of igf-1.a substitution glycine @ position thought introduce additional flexibility leading change of loop conformation, thereby disrupting hydrophobic interaction stabilises complex. @ amino acid position 98 unedited transcript contains lysine .this residue makes non specific interactions via aliphatic part of side chain glu-38 of igf-1.in edited version position arginine.the long side chain of thought able maintain these weak interactions

function

the edited region contains proposed heparin binding site , part of recognition sequence proteolytic cleavage.heparin binding inhibits cell binding , cell adhesion functions of protein. cleavage occurs @ amino acid position 97 reduces heparin binding modulates growth stimulatory activity of protein. since editing site occurs within proposed heparin binding region effects of editing may have implications heparin binding , proteolytic clevage , therefore have other affects downstream.since protein has been implicated in these processes believed editing might effect apoptosis, regulation of cell growth , angiogenesis.

functions in learning , memory

a study @ european neuroscience institute-goettingen (germany) found fear extinction-induced igf2/igfbp7 signalling promotes survival of 17- 19-day-old newborn hippocampal neurons. suggests therapeutic strategies enhance igf2 signalling , adult neurogenesis might suitable treat diseases linked excessive fear memory such ptsd. same group has found igfbp7 levels increased in alzheimer s disease , regulated via dna methylation. elevation of igfbp7 in wild type mice causes memory impairment. blocking igfbp7 function in mice develop alzheimer s disease-like memory impairment restores memory function. these data suggest igfbp7 critical regulator of memory consolidation , might used biomarker alzheimer s disease. targeting igfbp7 novel therapeutic avenue treatment of alzheimer s disease patients.