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However, previous research in animal models of ASD has shown increased glutamate receptor binding during adolescence instead of childhood, potentially reflecting compensatory mechanisms for earlier synaptic alterations [60]

53,73 The disulfide bond reduction and irreparable trimming of N -linked glycans generate degrons selectively modified with glycans such as Man 7 GlcNAc 2 , Man 6 GlcNAc 2 , or Man 5 GlcNAc 2 , which prevents substrate re-engagement with calnexin or calreticulin for nonproductive folding cycles