32 results on '"Segeren, Hendrika A"'
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2. Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.
3. Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance
4. Supplementary Figure from Genome-Protective Topoisomerase 2a-Dependent G2 Arrest Requires p53 in hTERT-Positive Cancer Cells
5. Supplementary Table from Genome-Protective Topoisomerase 2a-Dependent G2 Arrest Requires p53 in hTERT-Positive Cancer Cells
6. Data from Genome-Protective Topoisomerase 2a-Dependent G2 Arrest Requires p53 in hTERT-Positive Cancer Cells
7. Inferring single-cell protein levels and cell cycle behavior in heterogeneous cell populations
8. Mechanisms used by cancer cells to tolerate drug-induced replication stress
9. Transcription takes the wheel in the replication stress response: the road to drug sensitivity and resistance
10. Excessive E2F Transcription in Single Cancer Cells Precludes Transient Cell-Cycle Exit after DNA Damage
11. A distinctive requirement for p53 in the genome protective Topoisomerase 2a-dependent G2 arrest in hTERT positive cancer cells
12. Transcription takes the wheel in the replication stress response: the road to drug sensitivity and resistance
13. Oncogenic RAS sensitizes cells to drug-induced replication stress via transcriptional silencing of P53
14. Mechanisms used by cancer cells to tolerate drug-induced replication stress
15. Genome-Protective Topoisomerase 2a-Dependent G2 Arrest Requires p53 in hTERT-Positive Cancer Cells
16. Collection of cells for single-cell RNA sequencing using high-resolution fluorescence microscopy
17. A genome-wide RNAi screen identifies the SMC5/6 complex as a non-redundant regulator of a Topo2a-dependent G2 arrest
18. Oncogenic RAS sensitizes cells to drug-induced replication stress via transcriptional silencing of P53
19. Collection of cells for single-cell RNA sequencing using high-resolution fluorescence microscopy
20. Excessive E2F Transcription in Single Cancer Cells Precludes Transient Cell-Cycle Exit after DNA Damage
21. Excessive E2F transcription in single cancer cells precludes transient cell cycle exit after DNA damage
22. Cyclin F-dependent degradation of E2F7 is critical for DNA repair and G2-phase progression
23. A genome-wide RNAi screen identifies the SMC5/6 complex as a non-redundant regulator of a Topo2a-dependent G2 arrest
24. Cyclin F-dependent degradation of E2F7 is critical for DNA repair and G2-phase progression
25. Cyclin F-dependent degradation of E2F7 is critical for DNA repair and G2-phase progression
26. Cyclin F‐dependent degradation of E2F7 is critical for DNA repair and G2‐phase progression
27. Abstract B14: Feedback regulation between atypical E2Fs and APC/CCdh1 coordinates cell cycle progression.
28. A genome-wide RNAi screen identifies the SMC5/6 complex as a non-redundant regulator of a Topo2a-dependent G2 arrest.
29. Feedback regulation between atypical E2Fs and APC/C Cdh1 coordinates cell cycle progression
30. Feedback regulation between atypical E2Fs and APC /C Cdh1 coordinates cell cycle progression
31. Feedback regulation between atypical E2Fs and APC/ CCdh1 coordinates cell cycle progression.
32. Feedback regulation between atypical E2Fs and APC/CCdh1 coordinates cell cycle progression.
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