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JCI online early table of contents: Nov. 8, 2010
Date:11/8/2010

the protein Enigma promotes p53 degradation. Among the several lines of evidence that this mechanism has a role in tumor development and progression was the observation that Enigma promoted human cancer cell line survival and resistance to chemotherapy by suppressing p53-induced cell death in a mouse xenograft model. The authors therefore suggest that Enigma could be new therapeutic target for selective activation of the tumor suppressor p53.

TITLE: Enigma negatively regulates p53 through MDM2 and promotes tumor cell survival in mice

AUTHOR CONTACT:
Dong-Soo Im
Korea Research Institute of Bioscience and Biotechnology, Daejeon, South Korea.
Phone: 82.42.860.4172; Fax: 82.42.860.4597; E-mail: imdongsu@kribb.re.kr.

View this article at: http://www.jci.org/articles/view/42674?key=efd09435f3d59063fb1c


DERMATOLOGY: Improving wound healing in diabetes

Individuals with diabetes are at increased risk of wounds not healing properly, and this leads to over 72,000 amputations each year. Impaired generation of new blood vessels at the wound site is a key factor behind poor wound healing in these patients. This in turn is in part because cells responsible for making new blood vessellining cells (endothelial progenitor cells) are functionally impaired. A team of researchers, led by Alex Chen, at the University of Pittsburgh School of Medicine, Pittsburgh, has now identified a reason why endothelial progenitor cells are defective in diabetic mice.

In the study, endothelial progenitor cells were found to express decreased levels of the protein manganese superoxide dismutase and this reduced their ability to contribute to new blood vessel generation, thereby impairing wound healing. Importantly, gene therapy to replace manganese superoxide dismutase in endothelial progenitor cells fro
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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