https://www.selleckchem.com/products/danicopan.html Mechanically, LEF1-AS1 acted as a ceRNA for miR-543 and positively regulated engrailed homeobox 2 (EN2) expression. Down-regulation of miR-543 elevated GBM cell malignant behaviors, which was reversed by LEF1-AS1 knockdown. Meanwhile, the LEF1-AS1 inhibition could arrest the promoting effect of high-regulated EN2 on GBM cell aggressiveness and vice versa. In conclusion, our findings identified LEF1-AS1 as a ceRNA for miR-543 and showed that EN2 was positively regulated by LEF1-AS1. The LEF1-AS1/miR-543/EN2, as a novel ceRNA network, was implicated in the progression of GBM, which provided a novel insight for GBM treatment. Fatty acid binding protein 7 (FABP7) has a protective role in the central nervous system injury and regulates neurogenesis during brain development; however, its roles in neuronal injury and neurogenesis after cerebral ischemia have not been elucidated. In this study, the expression of FABP7 after ischemia was studied and the effects of genetic FABP7 inhibition on neuronal injury and neurogenesis after ischemia were investigated. Male FABP7 knockout (KO) mice on a C57BL/6J background and their wild-type (WT) littermates were subjected to transient forebrain ischemia for 20 min. There was no difference in the level of neuronal injury between WT and KO mice. FABP7 expression was observed in neural stem/progenitor cells and increased 7-10 days after ischemia, which was consistent with the peak of hippocampal neurogenesis. In the KO mice, neurogenesis was significantly decreased compared with WT mice under both physiological and ischemic conditions. Differentiation from newborn cells to immature neurons was activated in the KO mice, but there was no difference in the number of cells that differentiated into mature neurons. These findings imply that FABP7 expressed in neuronal stem/progenitor cells regulates the proliferation and maintenance of newborn cells. V.A method was developed and validated for