Production of a NF-¿B Deficient Microglial Animal Model

Abstract

Our goal is to determine how the nuclear factor-kappaB (NF-?B) signaling pathway is used in the communication between microglia and the progression of glioblastoma (GBM) cancer cells. The NF-?B signaling pathway is very important in normal immune system function and has been implicated in various types of cancers, including, GBM. GBM is the most common type of adult brain cancer, has altered NF-?B signaling, and is also characterized by a large population of microglia, the immune cell of the central nervous system. Based on our recent studies, we hypothesize that deleting the major transcription factor (p65) of the canonical NF-?B pathway in microglia would slow the progression of GBM. To test this hypothesis, we have developed a p65fl/fl/CX3CR1CreERtransgenic animal, which should lack microglial p65 after exposure to tamoxifen. We currently have heterozygous animals and will soon begin characterizing them to determine p65 deletion efficiency.