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This is likely due to a reduction of peptide interactions (mainly A5 Cagri ) with ECL3 that is a consequence of the engagement of the lipidated N-terminus with the top segment of TM5/ECL2, facilitating flexibility of ECL3

Cerebrospinal fluid and serum markers of inflammation in autism

While this association is not solely attributable to BDNF, the neurotrophin pathway is a leading mechanistic candidate

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