AI Article Synopsis
- Selective modulation of autophagy could be a beneficial therapy for cancer, but the lack of specific inhibitors has been a challenge.
- The ATG12-ATG5-ATG16L1 complex is crucial for the autophagy process, particularly in generating an important molecule called LC3-II.
- The study reveals that a stapled peptide from ATG16L1 effectively inhibits autophagy by strongly binding to ATG5, showing resistance to degradation, and demonstrating significant effects in cells.
Article Abstract
Selective modulation of autophagy is a promising therapeutic strategy, especially for cancer treatment. However, the lack of specific autophagy inhibitors limits this strategy. The formation of the ATG12-ATG5-ATG16L1 complex is essential for targeting the ATG12-ATG5 conjugate to proper membranes and to generate LC3-II for the progression of autophagy. Thus, targeting ATG5-ATG16L1 protein-protein interactions (PPIs) might inhibit early stage autophagy with high specificity. In this paper, we report that a stapled peptide derived from ATG16L1 exhibits potent binding affinity to ATG5, striking resistance to proteolysis, and significant autophagy inhibition activities in cells.
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| http://dx.doi.org/10.1021/jacs.2c07648 | DOI Listing |
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