Richard W. Bayliss

This study identifies the molecular mechanism by which hnRNPK activates Aurora-A kinase through specific residue interactions in the Y-pocket.

The paper designs and tests miniprotein inhibitors of Aurora-A kinase using structure-guided protein design, achieving high potency and selectivity over Aurora-B.

The paper identifies the DNA binding domain of TFIIIC5 as a key interaction site for N-myc and elucidates the molecular mechanism of their interaction using structural and biophysical methods.

This study presents structural models of the Aurora-A/Bora and Aurora-A/Bora/PLK1 complexes, revealing how Bora bridges Aurora-A activation and PLK1 substrate recognition.

This study identifies NEK7-mediated phosphorylation of cortactin as a mechanism by which EML4-ALK V3 enhances cell migration through actin cytoskeleton remodeling.

This study shows RAF inhibitors activate the integrated stress response via direct GCN2 activation, independent of ERK1/2, leading to ATF4 and CHOP expression.

This study generates genomic sequences for Galapagos iguanas to explore their evolutionary history and identify genes associated with marine adaptation, pigmentation, and DNA damage responses.

This study determines the structure of the ch-TOG-TACC3 interaction and shows that inhibiting it causes pericentriolar material fragmentation and delayed mitosis.

This study identifies Aurora-A as a CDK12-activating kinase in neuroblastoma, showing its role in transcription termination and tumor growth suppression.

This study uses NMR to analyze the structure, dynamics, and interactions of N-myc's transactivation domain, revealing phosphorylation sites and binding interactions.

The paper shows that TFIIIC binds MYCN and limits non-phosphorylated RNA Polymerase II accumulation at promoters, but does not affect MYCN-dependent gene expression or transcription elongation.