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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
No significant differences in the number of attacks received were detected between control and CCK-deficient KI mice (Fig
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Quantitative clinical pharmacology supports the bridging from i
