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1. Epigenetic modulators of B cell fate identified through coupled phenotype-transcriptome analysis

3. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

4. Data from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

5. Supplementary Figure from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

6. Data from CDK4/6 Inhibition Promotes Antitumor Immunity through the Induction of T-cell Memory

7. TableS1.xlsx from CDK4/6 Inhibition Promotes Antitumor Immunity through the Induction of T-cell Memory

8. Supplementary Figures from CDK4/6 Inhibition Promotes Antitumor Immunity through the Induction of T-cell Memory

9. RNA decay defines the response to transcriptional perturbation in leukaemia

10. Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

11. The PP2A-Integrator-CDK9 axis fine-tunes transcription and can be targeted therapeutically in cancer

12. CDK4/6 Inhibition Promotes Antitumor Immunity through the Induction of T-cell Memory

13. Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition

14. SUGAR-seq enables simultaneous detection of glycans, epitopes, and the transcriptome in single cells

15. Serine Biosynthesis Is a Metabolic Vulnerability in FLT3-ITD–Driven Acute Myeloid Leukemia

16. IL-15 Preconditioning Augments CAR T Cell Responses to Checkpoint Blockade for Improved Treatment of Solid Tumors

17. Temporal Analysis of Brd4 Displacement in the Control of B Cell Survival, Proliferation, and Differentiation

18. Epigenetic reprogramming of plasmacytoid dendritic cells drives type I interferon-dependent differentiation of acute myeloid leukemias for therapeutic benefit

19. 3002 – REPROGRAMMING OF SERINE METABOLISM IS A METABOLIC VULNERABILITY IN FMS-LIKE TYROSINE KINASE 3 (FLT3) MUTANT ACUTE MYELOID LEUKAEMIA

20. A PP2A-Integrator complex fine-tunes transcription by opposing CDK9

21. Reprogramming of serine metabolism is an actionable vulnerability in FLT3-ITD driven acute myeloid leukaemia

22. CDK13 cooperates with CDK12 to control global RNA polymerase II processivity

24. Genomic characterisation of Eμ-Myc mouse lymphomas identifies Bcor as a Myc co-operative tumour-suppressor gene

25. CDK13 cooperates with CDK12 to control global RNA polymerase II processivity.

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