{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T04:48:01Z","timestamp":1791175681517,"version":"4.1.0"},"reference-count":42,"publisher":"Rockefeller University Press","issue":"4","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,2,16]]},"abstract":"<jats:p>Because JunB is an essential gene for placentation, it was conditionally deleted in the embryo proper. JunB\u0394\/\u0394 mice are born viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease. Although JunB was reported to be a negative regulator of cell proliferation, junB\u0394\/\u0394 osteoclast precursors and osteoblasts show reduced proliferation along with a differentiation defect in vivo and in vitro. Mutant osteoblasts express elevated p16INK4a levels, but exhibit decreased cyclin D1 and cyclin A expression. Runx2 is transiently increased during osteoblast differentiation in vitro, whereas mature osteoblast markers such as osteocalcin and bone sialoprotein are strongly reduced. To support a cell-autonomous function of JunB in osteoclasts, junB was inactivated specifically in the macrophage\u2013osteoclast lineage. Mutant mice develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts. Thus, these data reveal a novel function of JunB as a positive regulator controlling primarily osteoblast as well as osteoclast activity.<\/jats:p>","DOI":"10.1083\/jcb.200308155","type":"journal-article","created":{"date-parts":[[2004,2,10]],"date-time":"2004-02-10T01:44:26Z","timestamp":1076377466000},"page":"613-623","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":185,"title":["Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects"],"prefix":"10.1083","volume":"164","author":[{"given":"Lukas","family":"Kenner","sequence":"first","affiliation":[{"name":"1Research Institute of Molecular Pathology (IMP), A-1030 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Astrid","family":"Hoebertz","sequence":"additional","affiliation":[{"name":"1Research Institute of Molecular Pathology (IMP), A-1030 Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F. 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