| First Author | Shinzawa M | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 414 |
| Issue | 4 | Pages | 773-8 |
| PubMed ID | 22005462 | Mgi Jnum | J:178720 |
| Mgi Id | MGI:5299981 | Doi | 10.1016/j.bbrc.2011.10.001 |
| Citation | Shinzawa M, et al. (2011) Splenic extramedullary hemopoiesis caused by a dysfunctional mutation in the NF-kappaB-inducing kinase gene. Biochem Biophys Res Commun 414(4):773-8 |
| abstractText | NF-kappaB-inducing kinase (NIK) plays critical roles in the development of lymph nodes and Peyer's patches, and microarchitecture of the thymus and spleen via NF-kappaB activation. Alymphoplasia (aly/aly) mice have a point mutation in the NIK gene that causes a defect in the activation of an NF-kappaB member RelB. Here, we developed a novel method to determine the aly mutation by genetic typing using PCR. This method facilitated the easy establishment of a congeneic aly/aly mouse line. Indeed, we generated a mouse line with aly mutation on a BALB/cA background (BALB/cA-aly/aly). BALB/cA-aly/aly mice showed significant splenomegaly with extramedullary hemopoiesis, which was not significant in aly/aly mice on a C57BL/6 background. Interestingly, the splenomegaly and extramedullary hemopoiesis caused by the aly mutation was gender-dependent. These data together with previous reports on extramedullary hemopoiesis in RelB-deficient mice suggest that NIK-RelB signaling may be involved in the suppression of extramedullary hemopoiesis in adult mice. |
