Methyl-CpG binding protein 1 (MBD1) regulates thing gene expression via a DNA methylation-mediated epigenetic mechanism. We now have previously demonstrated that MBD1 deficiency impairs adult neural stem/ progenitor cell (aNSC) differentiation and neurogenesis, but the underlying mechanism was unclear. Right here, Zosuquidar we present that MBD1 regulates the expression of several microRNAs in aNSCs and, particularly, that miR-184 is directly repressed by MBD1. Substantial ranges of miR-184 promoted proliferation but inhibited differentiation of aNSCs, whereas inhibition of miR-184 rescued the phenotypes connected to MBD1 deficiency. We even more discovered that miR-184 regulates the expression of Numb like (Numbl), a regarded regulator of brain improvement, by binding to the 3'-UTR of Numbl mRNA and affecting its translation. Expression of exogenous Numbl could rescue the aNSC defects that result from both miR-184 overexpression or MBD1 deficiency. Therefore, MBD1, miR-184, and Numbl type a regulatory network that helps handle the stability concerning proliferation and differentiation of aNSCs.