Mice transgenic for human TNF (hTNFtg mice), which develop a chronic inflammatory joint disease, were assessed for immunohistochemical evidence of activation of the three MAPK families (ERK, JNK and p38MAPKα).
From postnatal day P5 cochlear development is severely impaired in mutant Igf1−/− mice, which develop a smaller cochlea with an immature tectorial membrane.
The necessity of neurogenin 3 in the development of EC cells has been demonstrated in neurogenin 3−/− mice, which develop without any endocrine cells.
The proof of principle for the importance of STAT1 in impeding the development of tumors came from experiments with MMTV-neu tumor STAT1 null mice, which develop mammary tumors with shorter latency as compared to STAT1-proficient controls [ 8, 9, 11].
To test this idea, the team turned to so-called K/BxN mice, which develop inflammatory arthritis.
Two of the resulting BIN66 transgenic lines were crossed with APP23 mice, which develop severe central amyloidosis.
Here, we describe MXH10/Mo-lpr/lpr (MXH10/Mo/lpr) inbred mice, which develop systemic swelling of LNs up to 10 mm in diameter, allowing investigation of the topography of LNs and LVs.
Therefore, we also examined the effect of Beclin 1 gene dosage in Lck-Bax1 mice, which develop lymphoma with only about 50% penetrance at one year.
We crossed HCV-Tg mice that do not develop HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice.
Those that did develop tumors were not euthanized until 68 days after tumor challenge compared to the non-reconstituted mice which developed large tumors and were euthanized between 45 and 55 days after K562 cell injection.
