| First Author | Korkaya AK | Year | 2023 |
| Journal | Innate Immun | Volume | 29 |
| Issue | 8 | Pages | 171-185 |
| PubMed ID | 37828842 | Mgi Jnum | J:354084 |
| Mgi Id | MGI:7719069 | Doi | 10.1177/17534259231205993 |
| Citation | Korkaya AK, et al. (2023) Production of a p65(fl/fl)/LysMCre mouse model with dysfunctional NF-kappaB signaling in bone marrow-derived macrophages. Innate Immun 29(8):171-185 |
| abstractText | Here, we describe the production and characterization of a novel p65(fl/fl)/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-kappaB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65(fl/fl)/LysMCre mice do not exhibit differences in naive systemic immune profiles or colony forming units and time to death following Salmonella infection as compared to controls. Additionally, p65(fl/fl)/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies. |
