Conditional deletion of MAD2B in forebrain neurons enhances hippocampus-dependent learning and memory in mice.

ABSTRACT: Mitotic arrest deficient 2-like protein 2 (MAD2B) is not only a DNA damage repair agent but also a cell cycle regulator that is widely expressed in the hippocampus and the cerebral cortex. However, the functions of MAD2B in hippocampal and cerebral cortical neurons are poorly understood. In this study, we crossed MAD2B ^flox/flox and calcium/calmodulin-dependent protein kinase II alpha (Camk2a)-Cre mice to conditionally knock out MAD2B in the forebrain pyramidal neurons by the Cre/loxP recombinase system. First, RNA sequencing suggested that the differentially expressed genes in the hippocampus and the cerebral cortex between the WT and the MAD2B cKO mice were related to learning and memory. Then, the results of behavioral tests, includin

SUBMITTER: Cheng L 

PROVIDER: S-EPMC9538151 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature