Supplementary Figures S1 - S10, Tables S1 - S3 from Mutation-Specific RAS Oncogenicity Explains NRAS Codon 61 Selection in Melanoma

Figure S1. Generation of the LSL-N-RasQ61R allele. Figure S2. Conditional expression of N-Ras mutants does not alter melanocyte morphology. Figure S3. In both the heterozygous and homozygous state, NRasG12D fails to induce melanoma formation. Figure S4. Melanocyte-specific N-RASQ61R expression causes high penetrance nevus formation. Figure S5. Characteristics of Ras-mutant murine melanocytes and melanomas. Figure S6. Establishment and validation of TpLN61R/61R tumor cell lines. Figure S7. Binding of NRAS61R-mant-GMPPNP to PI3Kγ and RAF-RBD. Figure S8. NRASG12D and NRASQ61R similarly bind BRAF as measured by isothermal titration calorimetry. Figure S9. Proliferation of NRAS mutant human melanoma cell lines is not codon-specific. Figure S10. Activation of ERK and AKT in melanocytes is not codon-specific. Table S1. Frequency of canonical RAS mutations in human cancer. Table S2. Comparative stability of GMPPCP- and GDP- bound NRAS variants. Table S3. Summary of prior RAS-driven murine melanoma models.