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The PDI oxidization activity of Ero1L is regulated by an ER redox dependent disulfide bond formation via regulatory cysteines (C104 and C131 in hEro1L) 25,26

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Ironically, decrements of BDNF resulted in hyperconnectivity in the cortex and the decreased ability to prune synapses and with respect to ASD models, it was shown that reintroducing BDNF normalized those deficits, as the normalized variables also modified the chimpanzees social behavior and connectivity [59]

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