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1. Divergent WNT signaling and drug sensitivity profiles within hepatoblastoma tumors and organoids

2. Dual targeting of cancer metabolome and stress antigens affects transcriptomic heterogeneity and efficacy of engineered T cells

3. Trained innate immunity, long-lasting epigenetic modulation, and skewed myelopoiesis by heme

8. Antiviral responses induced by Tdap-IPV vaccination are associated with persistent humoral immunity to Bordetella pertussis

9. Blood monocyte transcriptome and epigenome analyses reveal loci associated with human atherosclerosis

10. Mutational mechanisms shaping the coding and noncoding genome of germinal center derived B-cell lymphomas

11. Antiviral responses induced by Tdap-IPV vaccination are associated with persistent humoral immunity to Bordetella pertussis

12. Dual targeting of cancer metabolome and stress antigens affects transcriptomic heterogeneity and efficacy of engineered T cells

13. Genome-wide modelling of transcription kinetics reveals patterns of RNA production delays

15. Extensive patient-to-patient single nucleus transcriptome heterogeneity in pheochromocytomas and paragangliomas.

16. The Organoid Cell Atlas

17. Dynamics of genome architecture and chromatin function during human B cell differentiation and neoplastic transformation

18. Rewiring of glucose metabolism defines trained immunity induced by oxidized low-density lipoprotein

20. Whole-genome fingerprint of the DNA methylome during human B cell differentiation

21. Inference of RNA Polymerase II Transcription Dynamics from Chromatin Immunoprecipitation Time Course Data

22. Dual targeting of cancer metabolome and stress antigens affects transcriptomic heterogeneity and efficacy of engineered T cells

24. International network of cancer genome projects

25. International network of cancer genome projects.

31. Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity

32. The reference epigenome and regulatory chromatin landscape of chronic lymphocytic leukemia

33. Supplementary Figure 1 from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors

34. Supplementary Tables S1-S4 and Supplementary Figures S1-S12 from Digitalis-like Compounds Facilitate Non-Medullary Thyroid Cancer Redifferentiation through Intracellular Ca2+, FOS, and Autophagy-Dependent Pathways

35. Supplementary Table 1 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

36. Data from Digitalis-like Compounds Facilitate Non-Medullary Thyroid Cancer Redifferentiation through Intracellular Ca2+, FOS, and Autophagy-Dependent Pathways

37. Supplementary Figure 1 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

38. Data from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

39. Supplementary Figure 4 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

40. Supplementary Figure Legends from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors

41. Supplementary Figure 2 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

42. Supplementary Figures 2 - 3 from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors

43. Data from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors

44. Supplementary Methods from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

45. Supplementary Figure 5 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

46. Supplementary Figure 3 from Death Receptor Pathway Activation and Increase of ROS Production by the Triple Epigenetic Inhibitor UVI5008

47. Supplementary Table 1 from Dual Promoter Usage as Regulatory Mechanism of let-7c Expression in Leukemic and Solid Tumors

48. Supplementary Table 2 from c-Myc Modulation and Acetylation Is a Key HDAC Inhibitor Target in Cancer

49. Supplementary Figure 3 from c-Myc Modulation and Acetylation Is a Key HDAC Inhibitor Target in Cancer

50. Supplementary Figure 5 from c-Myc Modulation and Acetylation Is a Key HDAC Inhibitor Target in Cancer

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