Kathleen M. Mulvaney

Figure S9. Colony formation assays of five cell lines treated with MEK1/2 inhibitor trametinib, PRMT5 inhibitor MRTX1719, or the combination across all drug concentrations are shown.

Figure S5. MTAP copy number and mRNA assessment of Cancer DepMap cell lines.

Figure S14. qRT-PCR of RAS target genes in RAS-MAPK active and RAS-MAPK wildtype cells.

Toxicity Study of drug combinations in vivo. Mouse body weight measurements.

Figure S16. Differential GSEA pathway analysis shows G2/M checkpoint is impacted by MTAC-PRMT5i and PRMT5 mRNA is repressed by treatment with either ERK1/2i or A/B/C-RAFi.

Figure S12. Differential GSEA by RNAseq reveals pathways modified by ERK1/2 inhibitor ulixertinib, MTAC-PRMT5i MRTX1719, or the combination.

Figure S15. Differential mRNA GSEA expression of A172 CDKN2A/MTAP null glioblastoma cells treated with MTAC-PRMT5i compared to control.

Figure S18. Protein level crosstalk between PRMT5 and RAS-MAPK signaling shows increased phospho-Fra1.

Figure S7. Colony formation assays of five cell lines treated with ERK1/2 inhibitor ulixertinib, PRMT5 inhibitor MRTX1719, or the combination across all drug concentrations are shown.

Figure S13. Differential mRNA GSEA pathway analysis shows KRAS SIGNALING UP in ERK1/2i and A/B/C-RAFi treatment.