Dustin Dovala

This paper introduces TRACERs, small-molecule drugs that silence transcription factors in cancer by recruiting repressor complexes, showing efficacy against ER and AR in breast and prostate cancer.

This study investigates how the two active sites of SARS-CoV-2 Mpro communicate and cooperate in catalysis using enzymatic assays, crystal structures, and engineered mutations.

This paper identifies a sulfinyl aziridine compound that selectively degrades MYC by targeting specific residues in its intrinsically disordered regions, demonstrating the potential of chiral small molecules for targeting undruggable proteins.

The paper identifies a small molecule that acts as a molecular glue degrader for CDO1 by recruiting it into the VHL E3 ligase complex, leading to its degradation.

This study investigates drug resistance mechanisms in SARS-CoV-2 Mpro caused by E166 mutations and their compensation by L50F, revealing structural and functional impacts on inhibitor binding and catalytic efficiency.

This study identifies hyperactive mutations in SARS-CoV-2 Mpro that increase enzyme activity and contribute to drug resistance, finding them more prevalent than binding-reducing mutations.

The paper identifies resistance mutations in SARS-CoV-2 main protease against nirmatrelvir and ensitrelvir using yeast screens, finding cross-resistant mutations and reduced enzyme function.

The paper performs a comprehensive mutational scan of SARS-CoV-2 Mpro to identify resistance mechanisms and guide inhibitor design.

This paper introduces a method to assess E3 ligase activity against neo-substrates using electrophilic probes, demonstrating its effectiveness with VHL and SPSB2.