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JCI table of contents: Jan. 24, 2008
Date:1/24/2008

stem/progenitor population in vivo is associated with enhanced bone regeneration in mice

AUTHOR CONTACT:
David T. Scadden
Massachusetts General Hospital, Boston, Massachusetts, USA.
Phone: (617) 726-5615; Fax: (617) 724-2662; E-mail: dscadden@mgh.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33102

ACCOMPANYING COMMENTARY TITLE: Bone building with bortezomib

AUTHOR CONTACT:
G. David Roodman
Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania, USA.
Phone: (412) 688-6571; Fax: (412) 688-6960; E-mail: roodmangd@upmc.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34734


NEUROBIOLOGY: Understanding a cause of Lou Gehrigs disease

Amyotrophic lateral sclerosis (ALS), often known as Lou Gehrigs disease, is the most common adult-onset motor neuron disease. Although most cases of ALS arise randomly, a sizeable proportion of individuals inherit the disease. Among these inherited cases, mutations in the SOD1 gene are the most frequently identified cause. A new study in mice, by John Engelhardt and colleagues at Iowa University, Iowa City, has identified a new mechanism by which SOD1 mutations associated with ALS can alter normal cellular function and trigger cell damage. As there is no known cure for ALS, the authors hope that these data might provide potential targets for the development of drugs to treat individuals with ALS caused by mutations in the SOD1 gene.

In the study, SOD1 was shown to regulate the production of the potentially dangerous oxygen radical superoxide by a protein known as Nox. In normal cells, SOD1 was found to bind and stabilize an activator of No
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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