6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Conditional inactivation of the mouse Wwox tumor suppressor gene recapitulates the null phenotype.

      Journal of Cellular Physiology
      Animals, Calcification, Physiologic, genetics, physiology, Female, Gene Expression Regulation, Developmental, Gene Targeting, Genes, Tumor Suppressor, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Animal, Osteosarcoma, pathology, Oxidoreductases, antagonists & inhibitors, Phenotype, Steroids, biosynthesis, Tumor Suppressor Proteins

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          WW domain-containing oxidoreductase (WWOX) is highly conserved in both human and murine. WWOX spans the second most common human chromosomal fragile site, FRA16D, and is commonly inactivated in multiple human cancers. Modeling WWOX inactivation in mice revealed a complex phenotype including postnatal lethality, defects in bone metabolism and steroidogenesis and tumor suppressor function resulting in osteosarcomas. For better understanding of WWOX roles in different tissues at distinct stages of development and in pathological conditions, Wwox conditional knockout mice were generated in which loxp sites flank exon 1 in the Wwox allele. We demonstrated that Cre-mediated recombination using EIIA-Cre, a Cre line expressed in germline, results in postnatal lethality by age of 3 weeks and decreased bone mineralization resembling total ablation of WWOX as in conventional null mice. This animal model will be useful to study distinct roles of WWOX in multiple tissues at different ages. Copyright © 2012 Wiley Periodicals, Inc.

          Related collections

          Author and article information

          Comments

          Comment on this article