Autor: |
David A. Scheinberg, Scott W. Lowe, Neal Rosen, Jedd D. Wolchok, Taha Merghoub, Ralph J. Garippa, Aaron Y. Chang, Qing Xiang, David Ulmert, Casey A. Jarvis, James E. Han, Patrizia Mondello, George Mo, Ron S. Gejman, Sadna Budhu, Eusebio Manchado, Claire Y. Oh, Elliott J. Brea |
Rok vydání: |
2023 |
Popis: |
Supplementary Table S1. MSK Memorial Hospital IMPACT genomic sequencing data for the JMN human mesothelioma cell line. Supplementary Table S2. Sh RNA used. Supplementary Table S3. List of antibodies used. Supplementary Table S4. Top 5 negative regulatory and top 5 positive regulatory kinase genes that were hits from the screen for regulating surface HLA-A expression. Supplementary Figure S1. Knockdown of HLA-A causes resistance to antibody dependent cellular cytotoxicity by the ESK-M mAb. Supplementary Figure S2. Coordinated regulation of total surface HLA-A, B, and C with knockdown of either MAP2K1 of EGFR. Supplementary Figure S3. Validation of MAP2K1, EGFR, and RET as negative kinase regulators in mesothelioma cell lines. Supplementary Figure S4. DDR2 and MINK1 acts as positive regulators of surface HLA-A. Supplementary Figure S5. Treatment with IFN gamma and/or kinase inhibitors, afatinib or trametinib, on cells with mutant EFGR (H1975) or mutant BRAF (SK-Mel5 and UACC257). Supplementary Figure S6. Viability of JMN after treatment with MEKi trametinib and EGFRi Afatinib. Supplementary Figure S7. Titration of trametinib to determine optimal inhibition of MEK using pERK as a marker of inhibition. Supplementary Figure S8. JMN was treated with 50 nM trametinib and lysate was analyzed as in Figure 4C at different time points. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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