Phosphorylation: The Molecular Switch of Double-Strand Break Repair

Repair of double-stranded breaks (DSBs) is vital to maintaining genomic stability. In mammalian cells, DSBs are resolved in one of the following complex repair pathways: nonhomologous end-joining (NHEJ), homologous recombination (HR), or the inclusive DNA damage response (DDR). These repair pathways rely on factors that utilize reversible phosphorylation of proteins as molecular switches to regulate DNA repair. Many of these molecular switches overlap and play key roles in multiple pathways. For example, the NHEJ pathway and the DDR both utilize DNA-PK phosphorylation, whereas the HR pathway mediates repair with phosphorylation of RPA2, BRCA1, and BRCA2. Also, the DDR pathway utilizes the kinases ATM and ATR, as well as the phosphorylation of H2AX and MDC1. Together, these molecular switches regulate repair of DSBs by aiding in DSB recognition, pathway initiation, recruitment of repair factors, and the maintenance of repair mechanisms

Supplementary Table S3 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Normalization constants (mRNA_normalization_factors) and mean squared error for each sample computed based on selected housekeeping genes (HK_MSE).</p

Supplementary Figure S5 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Supplemental Figure 5. scRNAseq analysis of human NF1-associated MPNST.</p

Supplementary Table S9 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

PathView normalized signature scores for biological pathways relevant to tumor progression, immune response and tumor microenvironment for each sample.</p

Supplementary Figure S7 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Supplemental Figure 7. Gene expression analysis of harmonized RNAseq data from normal nerve and MPNST samples obtained from GTEx and TCGA.</p

Supplementary Table S2 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Probes excluded due to low signal (below background).</p

Supplementary Table S11 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

List of Normal Nerve and MPNST samples obtained from XenaBrowser.net</p

Supplementary Figure S3 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Supplemental Figure 3.  PNF, ANNUBP, and MPNST exhibit distinct global gene expression programs.</p

Supplementary Table S12 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Differentially expressed genes comparing GTEx Normal Nerve and TCGA MPNST obtained from XenaBrowser.net</p

Supplementary Figure S10 from Spatial Gene-Expression Profiling Unveils Immuno-oncogenic Programs of NF1-Associated Peripheral Nerve Sheath Tumor Progression

Supplemental Figure 10. Survivin inhibition with LQZ-7I abrogates viability of human MPNST and murine primary Schwann cell precursors.</p