ArticleCells2026
Challenges in Developing a Microglial NF-Kappa B Conditional Mouse Model for Glioblastoma Studies.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Tumor microenvironments (TME) play a crucial role in the formation, progression, and drug resistance of many cancers, including glioblastoma (GBM). Microglia are the resident innate immune cells of the central nervous system and are associated with brain cancers like GBM. However, there are limited studies about the specific effects that microglia have on GBM tumors. One possible way to reduce GBM tumor progression is by targeting key signaling pathways in microglia, such as the nuclear factor-kappa B (NF-κB) signaling pathway, which has been implicated in both microglia/macrophage phenotype polarization and in brain cancers like GBM. Therefore, this study aimed to produce a p65fl/fl/CX3CR1creER/+ mouse model, an inducible p65 knockout mouse model to be used for studying how inhibition of canonical NF-κB signaling in microglia affects GBM tumors. Following tamoxifen administration to the mouse, p65, a transcription factor of the canonical NF-κB pathway, should be deleted in microglia due to activation of a Cre recombinase (creER) under the control of the CX3CR1 promoter. This mouse model was characterized to determine whether the
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.