| Autor: |
Jean-Pierre J. Issa, Donald L. Gill, Stephen B. Baylin, Ying Cui, Jaroslav Jelinek, Andrew J. Andrews, Ryan A. Henry, Magid Abou-Gharbia, Wayne E. Childers, Woonbok Chung, Saira Ahmed, Vazganush Gharibyan, Elisha J. Dettman, Sarah Dumont, Gabriel G. Malouf, Judith Garriga, Priyanka Madireddi, Annie Beaudry, Youjun Wang, Justin T. Lee, Noël J.-M. Raynal |
| Rok vydání: |
2023 |
| DOI: |
10.1158/0008-5472.22410428 |
| Popis: |
Supplementary Figure S1. Drug screening based on the measurement of GFP fluorescence by flow cytometry. Supplementary Figure S2. Dose response curves of GFP reactivation after cardiac glycosides treatment. Supplementary Figure S3. Tumor suppressor genes reactivation after treatment with validated hits. Supplementary Figure S4. Analysis DNA methylation and histone modifications following treatments with validated hits. Supplementary Figure S5. Characterization of Ca2+ fluxes in YB5 and HEK293 cells. Supplementary Figure S6: Tumor suppressor gene reactivation is dependent on CamK activity. Supplementary Figure S7. Promoter occupancy of MeCP2 is decreased after cardiac glycoside treatment. Supplementary Figure S8: Specificity of MeCP2 antibody. Supplementary Figure S9: Assessing the specificity of MeCP2 redistribution after proscillaridin treatment. Supplementary Figure S10. Percentage of YB5 cells expressing GFP after drug treatment is significantly reduced after leptomycin treatment. Supplementary Figure S11. Cell viability assays show that drug induced toxicity is dependent on CamK activity in SW48 colon cancer cell line. Supplementary Figure S12. Cell viability assays show that drug induced toxicity is dependent on CamK activity in K562 leukemia cell line. Supplementary Figure S13. Cell viability assays show that drug induced toxicity is dependent on CamK activity in HL-60 leukemia cell line. Supplementary Figure S14. Scheme describing proposed mechanism of action of newly identified candidate epigenetic drugs. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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