The content you've requested is available without charge only to active Sigma Xi members and
If you are an active member or an individual subscriber, please log in now in order to access this article.
If you are not a member or individual subscriber, you can:
Most diseases with a genetic basis involve a mutation in some gene that affects how much of its protein is made or how well that protein works. However, a growing body of research indicates that this scenario may not be universally true. Conn and Janovick explain that many diseases, including cystic fibrosis, Alzheimer's and diabetes, are products of improperly folded—but potentially functional—proteins. When the authors added a template for correct folding (which they call a pharmacoperone) to a cell with such a "mutant" protein, the cellular defect was fixed. This remedy suggests that the rescue of a person's own misfolded proteins may be an alternative to the broader physiological tinkering (and attendant side effects) caused by most of the current drugs used to treat these diseases.
Connect With Us:
An early peek at each new issue, with descriptions of feature articles, columns, and more. Every other issue contains links to everything in the latest issue's table of contents.News of book reviews published in American Scientist and around the web, as well as other noteworthy happenings in the world of science books.
To sign up for automatic emails of the American Scientist Update and Scientists' Nightstand issues, create an online profile, then sign up in the My AmSci area.
JSTOR, the online academic archive, contains complete back issues of American Scientist from 1913 (known then as the Sigma Xi Quarterly) through 2005.
The table of contents for each issue is freely available to all users; those with institutional access can read each complete issue.
View the full collection here.
Receive notification when new content is posted from the entire website, or choose from the customized feeds available.