Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
Degradation of dysfunctional proteins using proteolysis-targeting chimeras (PROTACs) has shown great promise in targeting previously undruggable proteins. However, aberrant protein degradation is a pathogenic mechanism in diseases such as cystic fibrosis and some forms of cancer. Therefore, targeted protein stabilization, rather than degradation, would be of therapeutic benefit in these cases. Writing in Nature Chemical Biology, Henning et al. describe the development of heterobifunctional molecules analogous to PROTACs capable of targeted protein stabilization, known as deubiquitinase-targeting chimeras (DUBTACs). They demonstrate the use of a DUBTAC to stabilize and restore the function of an unstable mutant form of the chloride channel CFTR, the aberrant degradation of which is linked to cystic fibrosis pathogenicity.