JCI table of contents -- Februa...( e to the ability of gentamicin to induc...)

e to the ability of gentamicin to induce the production of functional CFTR protein. This study suggests that the ability of an individuals affected cells to destroy nonsense mRNA determines how responsive CF patients with the W1282X mutation are likely to be to treatment with gentamicin. Such observations might also extend to other genetic disorders in which mutations causing the cellular machinery to prematurely stop making protein have been identified, such as Duchenne muscular dystrophy.

TITLE: Nonsense-mediated mRNA decay affects nonsense transcript levels and governs response of cystic fibrosis patients to gentamicin

AUTHOR CONTACT:
Batsheva Kerem
The Hebrew University of Jerusalem, Jerusalem, Israel.
Phone: +972-2-6585689; Fax: +972-2-6584810; E-mail kerem@cc.huji.ac.il.

View the PDF of this article at: https://www.the-jci.org/article.php?id=28523

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ONCOLOGY: HMGA1 stops p53 in its tracks in cancer cells

Overexpression of a protein known as HMGA1 has been associated with many types of cancer in humans. Previous studies have shown that HMGA1 decreases the ability of p53 to inhibit cell death by a process known as apoptosis; inhibition of p53-mediated apoptosis causes tumors to develop in both animals and humans. However, precisely how HMGA1 mediates its pro-tumorigenic effects on p53 have not been clearly established. Now, researchers from the Istituto Nazionale dei Tumori Regina Elena, Italy, show that in human cancer cell lines, HMGA1 inhibits p53-mediated apoptosis by interfering with the protein HIPK2, which helps p53 initiate apoptotic cell death.

In the study, which appears online on February 8 in advance of publication in the March print issue of the Journal of Clinical Investigation, Silvia Soddu and colleagues found that overexpression of HMGA1 inhibited p53-
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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
8-Feb-2007

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