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Furthermore, we found that KCNQ2-5 agonist Retigabine and AAV-mediated restoration of KCNQ5 expression level could partially reverse the defects of social ability in Gadd45a KO mice, which indicated the impaired function of K+ channels may be the major contributor to the autistic phenotype in our mouse model

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Treatment with 5 M C1-27 for 24 h resulted in an increase in the S-phase population, with a concomitant decrease in the G0/G1 population (Fig