J. A. Marto

This paper describes a new mechanism for molecular glue degraders called template-assisted covalent modification, showing how BRD4 degraders recruit CUL4DCAF16 to degrade BRD4.

This paper develops a covalent inhibitor of the YAP-TEAD complex, demonstrating its ability to suppress Hippo signaling defects and inhibit cancer cell growth.

This study identifies a non-canonical glutamine metabolism pathway in DLBCLs where mitochondrial pyruvate supports glutaminolysis and proliferation, particularly in solid extracellular matrix environments.

The paper identifies IER5 as a Notch-induced DNA-damage response gene required for squamous cell differentiation and shows its interaction with PP2A subunit PPP2R2A.

Sulfopin, a selective Pin1 inhibitor, reduces tumor initiation and growth in neuroblastoma models by targeting c-Myc pathways.

The paper identifies a mechanism by which RNA granules are transported via direct interaction with KIF5A/KLC1 motors, preventing axon degeneration in CMT models.

The paper shows STRIPAK directs PP2A to dephosphorylate MAP4K4, promoting oncogenic transformation via YAP1 activation.

This study identifies THZ-P1-2, a covalent pan-PI5P4K inhibitor, showing efficacy in AML/ALL cell lines and autophagy disruption, supporting PI5P4Ks as therapeutic targets in cancer.

This study identifies the molecular mechanism by which NRARP inhibits Notch signaling by binding to the NTC complex and disrupting its function.

This study develops a covalent inhibitor of gut bacterial bile salt hydrolases, showing it reduces BSH activity and deconjugated bile acids in mice.

The paper analyzes RNA polymerase II elongation complex dynamics in vitro using mass spectrometry, revealing changes in factor binding and phosphorylation patterns over time.