Characterization of p80HT transgenic mice. (A) Schematic diagram of NF-κB2 p100, p52, and representative tumor-derived mutants. The arrow indicates the cleavage site in p100 that gives rise to p52. RHD, Rel-homology domain; DD, death domain. (B) Immunoblot analysis of tissue-specific expression of p80HT and p52 using an antibody against the N-terminal region of human NF-κB2. The star indicates a degraded p80HT product. Levels of α-tubulin are shown as loading control. BM, bone marrow; LN, lymph node; Sp, spleen; Th, thymus; H, heart; K, kidney; Li, liver; Lu, lung; St, stomach; T, splenic T cells; B, splenic B cells. (C) Electrophoretic mobility shift assay for κB-binding activity in nuclear extracts of splenic lymphocytes from p80HT transgenic (Tg) and wild-type (WT) mice. Two κB-binding complexes containing either NF-κB2 or NF-κB1 are indicated based on antibody-mediated supershift. The NF-κB2 complex was disrupted by anti-RelA and, to a lesser degree, by anti-c-Rel. Preimmune rabbit IgG was used as control.