Autor: |
William L. Carroll, Nikki A. Evensen, Aristotelis Tsirigos, Xiaotu Ma, Jinghui Zhang, Patrick A. Brown, Mignon L. Loh, Jun J. Yang, Kjeld Schmiegelow, David T. Teachey, Tori J. Fuller, Takaya Moriyama, Harrison L. Kilberg, Hannah Fay, Anita Qualls, Ashfiyah Chowdhury, Shella Saint Fleur-Lominy, Gunjan Sethia, Sonali Narang, Jason Saliba, Joanna Pierro |
Rok vydání: |
2023 |
Popis: |
S1. Schematic diagram of NSD2 isoform indicating domains, the location of amino acid E1099 within the SET domain, and the targets of the shRNAs. S2. NSD2 Overexpression in B-ALL Cell Lines Does Not Impart Clonal Advantage. S3. Overexpression of REIIBP in B-ALL Cell Lines Does Not Impart Clonal Advantage. S4. Knockdown of WT NSD2 in B-ALL Cell Lines Does Not Lead to Phenotypic Differences. S5. Knockdown of NSD2 in RS4;11 and RCH-ACV lines leads to increased chemosensitivity. S6. Sensitivity to 6-MP Upon Knockdown of NSD2 in RS4;11 is Not Depedent of Level of Knockdown. S7. Knockdown of NSD2 in WT B-ALL Cell Lines Does Not Lead to Increased Sensitivity. S8. NSD2 WT and EK Overexpression in B-ALL Cell Lines Leads to Distinct Genetic Signature Unique to Each Cell Line. S9. NSD2 WT and EK Overexpression in B-ALL Cell Lines Leads to Distinct Epigenetic Signature Resulting in Gene Expression Changes. S10. NSD2 Knockdown in Mutant B-ALL Cell Lines Leads to Distinct Genetic Signature Unique to Each Cell Line. S11. ATAC peaks significantly correlate with gene expression for RS4;11 and RCH-ACV cell lines. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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