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.
Two of the resulting BIN66 transgenic lines were crossed with APP23 mice, which develop severe central amyloidosis.
A few years ago, Dr. Ellen Heber-Kanz, an immunologist at the Wistar Institute in Philadelphia, was conducting an experiment with those mice, which develop a disease similar to lupus.
When the protein, called GDF-11, was injected into old mice, which develop thickened heart walls in a manner similar to aging humans, the hearts were reduced in size and thickness, resembling the healthy hearts of younger mice.
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.
Sca-1 mice, which develop fewer MSCs, were crossed with Apc wt/1638N) mice.
To test this idea, the team turned to so-called K/BxN mice, which develop inflammatory arthritis.
To address this question, we used Kras LA1) mice, which develop lung adenocarcinomas from somatic activation of a Kras(G12D) allele.
Ultimately they were tested in Apc1638N mice, which develop desmoid tumors, as well as in wild type mice subjected to full thickness skin wounds.
