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1. Author Correction: Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells

4. Abstract 464: AAC-11 survival pathways as therapeutic target in cancer: AAC-11 leucine-zipper domain derived peptides exert potent antitumor effects and exhibit favorable stability, pharmacokinetic and toxicology profiles

5. Data from Deletion 6q Drives T-cell Leukemia Progression by Ribosome Modulation

6. Table S4 from Deletion 6q Drives T-cell Leukemia Progression by Ribosome Modulation

7. Supplementary Data from Deletion 6q Drives T-cell Leukemia Progression by Ribosome Modulation

11. Data from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

12. Data from BCL-2 and Mutant NRAS Interact Physically and Functionally in a Mouse Model of Progressive Myelodysplasia

13. Supplementary Procedures, Figures 1-4 from BCL-2 and Mutant NRAS Interact Physically and Functionally in a Mouse Model of Progressive Myelodysplasia

14. Supplementary Table 1 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

15. Supplementary Figure 1 Legend from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

16. Supplementary Figure 1 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

17. Supplementary Table 2 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

18. Supplementary Table 5 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

19. Supplementary Table 3 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

20. Supplementary Table 4 from Reactive Oxygen Species, DNA Damage, and Error-Prone Repair: A Model for Genomic Instability with Progression in Myeloid Leukemia?

21. Major histocompatibility class I antigenic peptides derived from translation of pre-mRNAs generate immune tolerance

22. BCL-2 inhibition with ABT-737 prolongs survival in an NRAS/BCL-2 mouse model of AML by targeting primitive LSK and progenitor cells

23. Localization of the NRAS:BCL-2 complex determines anti-apoptotic features associated with progressive disease in myelodysplastic syndromes

25. Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells

26. Exploration of nuclear body-enhanced sumoylation reveals that PML represses 2-cell features of embryonic stem cells

27. BCL-2 Inhibitor ABT-737 Effectively Targets Leukemia-Initiating Cells with Differential Regulation of Relevant Genes Leading to Extended Survival in a NRAS/BCL-2 Mouse Model of High Risk-Myelodysplastic Syndrome

29. Unbiased in vivo exploration of nuclear bodies-enhanced sumoylation reveals that PML orchestrates embryonic stem cell fate

30. Prophylactic and therapeutic antileukemic effects induced by the AAC-11-derived Peptide RT53

31. PML-RARA-targeted DNA vaccine induces protective immunity in a mouse model of leukemia

33. Nuclear processing of nascent transcripts determines synthesis of full-length proteins and antigenic peptides

42. Deletion 6q Drives T-cell Leukemia Progression by Ribosome Modulation

43. BCL-2 Inhibitor Venetoclax (ABT-199) and MEK Inhibitor GDC-0973 Synergise to Target AML Progenitors and Overcome Drug Resistance with the Use of PET Scanning in a Mouse Model of HR-MDS to Monitor Response to Treatment

44. Studies in an Early Development Window Unveils a Severe HSC Defect in both Murine and Human Fanconi Anemia

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