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Using animal models, Cleveland Clinic researchers discovered that during this neuroinflammatory process, the epigenetic modification of NLGN1 disrupts the synaptic network in the brain, which is responsible for developing and maintaining memories.
So extending the assumption of X chromosome evolution from autosome we can assume that paralog of X-linked genes must be on autosome and should be involved in the same disorder; like ARHGEF6 (X chromosome) has its paralog ARHGEF3 and ARHGEF4 on autosome; similarly NLGN3, NLGN4 on X -chromosome has paralog NLGN1 and NLGN2 on autosome.
Genes involved in neuronal cell adhesion (including NRXN1, CNTN4, NLGN1, ASTN2) were enriched with copy number variation in ASD cases, compared with controls, as were genes involved in ubiquitin degradation (including UBE3A, PARK2, RFWD2, and FBXO40).