Jennifer M. Binning

This study shows that high-risk HPV E7 proteins require inactivating both RB1 and PTPN14 to extend keratinocyte lifespan, while low-risk E7 needs PTPN14 inactivation alone.

This study uses ancestral protein reconstruction to uncover the molecular mechanism of substrate specificity in FN3K and KT3K enzymes, revealing an allosteric network that modulates substrate recognition.

This study identifies QPRT as a non-canonical apoptosis regulator in NSCLC that suppresses caspase-3 activation, independent of its role in NAD biosynthesis, suggesting it as a therapeutic target.

This study develops a PROTAC that degrades HPV E6 protein, reducing tumor burden in a mouse model and showing immune dependence.