Mutations Can't Go All The Way In Paget Disease
In a study appearing online in advance of publication in the January print issue of the Journal of Clinical Investigation, Noriyoshi Kurihara and colleagues from the VA Pittsburgh Healthcare System show that expression of the p62P392L mutation causes abnormal development of human bone cells in vitro and mouse bone cells in vivo but does not cause a Padget-like disease in mice. Specifically, expression of p62P392L in the precursors of human bone cells known as osteoclasts (the cells that destroy bone) caused them to be more responsive to factors that drive osteoclast development. Similarly, expression of p62P392L in osteoclast-lineage cells in mice resulted in increased numbers of osteoclasts. Although increased numbers of osteoclasts is a feature of Paget disease, it is not the full range of characteristics. This study therefore suggests that although mutations in p62 predispose an individual to developing Paget disease, other factors are required for the full development of Paget disease.
TITLE: Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget disease
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Article adapted by Start Sanatate from original press release.
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JCI table of contents: Dec. 21, 2006
AUTHOR CONTACT:
Noriyoshi Kurihara
VA Pittsburgh Healthcare System and University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Contact: Karen Honey
Journal of Clinical Investigation
Mutaþii nu poate merge tot drumul în boala Paget - Mutations Can't Go All The Way In Paget Disease - articole medicale engleza - startsanatate