Acute pharmacological degradation of ERK5 does not inhibit cellular immune response or proliferation
Collaborators in the Gray lab at Stanford developed INY-06-061, a potent and selective heterobifunctional degrader of ERK5 to be used as a tool for validating phenotypes associated with ERK5 ablation. Results from a standard PRISM assay using the PR800 cell set verified a lack of dependency on ERK5 expression for cell growth (as no cell […]
Results from a standard PRISM assay using the PR500 cell set suggested that the novel compound, XL177A, acts by USP7 inhibition and that sensitivity to USP7 inhibition is associated with the mutational status of TP53. This study also found two pediatric cancers, Ewing sarcoma, and malignant rhabdoid tumor, were sensitive to XL177A.
Results from a standard PRISM assay using the PR1000 cell set showed INK4 overexpression (along with RB1 loss) to be among the top genomic alterations associated with resistance to CDK4/6 inhibition with Palbociclib. This paper also identified a new strategy to enhance inhibition of CDK4/6 kinases.