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4. Systematic evaluation of AML-associated antigens identifies anti-U5 SNRNP200 therapeutic antibodies for the treatment of acute myeloid leukemia

8. SETBP1 is dispensable for normal and malignant hematopoiesis

10. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

11. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

12. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

13. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

14. Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

15. Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

16. Table S1 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

17. Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

18. Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

19. Table S4 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

20. Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

21. Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

22. Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

23. Table S4 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

24. Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

25. Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

26. Table S1 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

27. Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

28. Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

29. Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

30. Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

31. Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

32. Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

33. Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

36. Systematic Evaluation of AML-Associated Antigens Identifies Novel Anti-U5 snRNP200 Therapeutic Antibodies for the Treatment of AML

37. Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

38. Exploring the mechanistic link between SF3B1 mutation and ring sideroblast formation in myelodysplastic syndrome

39. Aberrant EVI1 splicing contributes to EVI1-rearranged leukemia

42. MDS cells impair osteolineage differentiation of MSCs via extracellular vesicles to suppress normal hematopoiesis

44. Impaired RAS Proteolysis Drives Clonal Hematopoietic Transformation

46. ASXL1 mutations are associated with distinct epigenomic alterations that lead to sensitivity to venetoclax and azacytidine

47. Minor intron retention drives clonal hematopoietic disorders and diverse cancer predisposition

48. Mutant ASXL1 induces age-related expansion of phenotypic hematopoietic stem cells through activation of Akt/mTOR pathway

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