| Autor: |
Madhobi Sen, Wang, Xin, Feda Hamdan, Jacobe Rapp, Eggert, Jessica, Kosinsky, Robyn, Wegwitz, Florian, Kutschat, Ana, Younesi, Fereshteh, Gaedcke, Jochen, Grade, Marian, Hessmann, Elisabeth, Papantonis, Argyris, StrÓ§Bel, Philipp, Johnsen, Steven |
| Rok vydání: |
2019 |
| DOI: |
10.6084/m9.figshare.8299016.v1 |
| Popis: |
Figure S1. Expression of BAF complex subunits in the four cell lines used in this study (a). Mutual exclusivity of ARID1A and KRAS (all and specifically at residues G12 and G13) mutations in the colorectal adenocarcinoma patient cohort from the TCGA PanCancer Atlas (b). Levels of pERK and JUND in Parental and ARID1A KO DLD1 cells (c). HSC70 was used as a loading control. The top 10 GO terms enriched for genes downregulated by ARID1A KO in the HCT116, DLD1, and COLO320 cell lines (d). Figure S2. Transcription factors that colocalize at all ARID1A-bound sites. These include several AP1 transcription factors (a). The AP1 binding motif is significantly enriched at all ARID1A-occupied regions (b). At all ARID1A-bound enhancers there is a reduction of SMARCA4 and SMARCC1 occupancy upon the loss of ARID1A (c). ATAC-seq signal remains unchanged and H3K27ac reduces significantly (c). (PDF 126 kb) |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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