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Protein degradation

Traditional approaches in the development of small-molecule drugs typically aim to inhibit the biochemical activity of functional protein domains. In contrast, targeted protein degradation aims to reduce overall levels of disease-relevant proteins. Control of human protein-degradation machinery revealed. A long-standing puzzle in molecular biology is how the enzyme USP14 is activated by the proteasome and regulates protein degradation. Over the past five years, targeted protein degradation has been a hotbed of public and private sector investment. PROTACs are molecules which cause protein degradation. Protein degradation is akin to gene knockout: it can provide insight into the cellular functions of proteins. Simultaneous binding of a target protein and an E3 ligase by a PROTAC within a key ternary complex facilitates ubiquitylation of the target protein. We have generated a set of dual-reporter human cell lines and devised a chase protocol to quantify proteasomal degradation of a ubiquitin fusion degradation (UFD) substrate, a ubiquitin ligase CRL2VHL substrate, and a ubiquitin-independent substrate

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