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|Title:||Insulin- like growth factor- II ( IGF- II) and IGF- II analogs with enhanced insulin receptor- a binding affinity promote neural stem cell expansion|
|Citation:||Journal of Biological Chemistry, 2014; 289(8):4626-4633|
|Publisher:||American Society for Biochemistry and Molecular Biology|
|Amber N Ziegler, Shravanthi Chidambaram, Briony E. Forbes, Teresa L. Wood and Steven W. Levison|
|Abstract:||The objective of this study was to employ genetically engineered IGF-II analogs to establish which receptor(s) mediate the stemness promoting actions of IGF-II on mouse subventricular zone neural precursors. Neural precursors from the subventricular zone were propagated in vitro in culture medium supplemented with IGF-II analogs. Cell growth and identity were analyzed using sphere generation and further analyzed by flow cytometry. F19A, an analog of IGF-II that does not bind the IGF-2R, stimulated an increase in the proportion of neural stem cells (NSCs) while decreasing the proportion of the later stage progenitors at a lower concentration than IGF-II. V43M, which binds to the IGF-2R with high affinity but which has low binding affinity to the IGF-1R and to the A isoform of the insulin receptor (IR-A) failed to promote NSC growth. The positive effects of F19A on NSC growth were unaltered by the addition of a functional blocking antibody to the IGF-1R. Altogether, these data lead to the conclusion that IGF-II promotes stemness of NSCs via the IR-A and not through activation of either the IGF-1R or the IGF-2R.|
|Keywords:||Stem cells; central nervous system; cell proliferation; self-renewal; insulin receptor; neurodevelopment; insulin; receptor tyrosine kinase|
|Rights:||Copyright 2014 by The American Society for Biochemistry and Molecular Biology, Inc.|
|Appears in Collections:||Medicine publications|
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