Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 3 December 2004:
Vol. 306. no. 5702, p. 1645
DOI: 10.1126/science.306.5702.1645m
Prev | Table of Contents | Next

This Week in Science

One approach to circumventing the dystrophin mutation that is associated with muscular dystrophy is to "skip" the exons containing the mutation and produce a truncated RNA that still preserves protein function. Goyenvalle et al. (p. 1796, published online 4 November 2004) have shown that a single treatment with an adeno-associated viral vector containing a modified U7 snRNA caused exon skipping in the dystrophin mRNA precursor. When injected into mdx mice, whole muscles contained enough skipped mRNA to allow near normal levels of synthesis of dystrophin and the mice showed restored mechanical properties and resilience of muscle fibers.




To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)