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Such phosphorylation leads to the blockade of the tyrosine residues in IRSs, to which the insulin and IGF-1 receptors phosphorylate to activate IRSs and consequently commence the signalling cascade [185, 192], as comprehensively discussed above

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Several mechanistic models have been rendered to explain how the small neurotrophin peptidomimetics and non-peptide ligands can elicit the TrkB-dependent cellular response, although the exact structural basis for peptidomimetics/Trks interaction and subsequent activation remain obscure 44