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| Transgenic mice specifically lacking JunB expression in the myeloid lineage develop a transplantable myeloproliferative disease eventually progressing to blast crisis and mice reconstituted with ES cell-derived junB-/- fetal liver cells also develop a myeloproliferative disease  | |
JunBDelta/Delta mice are viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease |
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mice with specific inactivation of Junb in the macrophage-osteoclast lineage develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts |
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inducible epidermal deletion of JunB and c-Jun in adult mice leads to a phenotype resembling the histological and molecular hallmarks of psoriasis, including arthritic lesions |
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Depletion of JunB by siRNA abrogates TGF-& |
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946;-induced disruption of cell-cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins |