33 results on '"Yan, Xiaomei"'
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2. Stress hematopoiesis reveals abnormal control of self-renewal, lineage bias, and myeloid differentiation in Mll partial tandem duplication (Mll-PTD) hematopoietic stem/progenitor cells
3. RUNX1 Mutation Leads to Megakaryocyte-Primed Hematopoietic Stem Cell Expansion and Familial Platelet Disorder
4. This Is a Title in Title Case: Prediction of CML Evolution By Telomere Length Analysis at the Single-Chromosome Level
5. Myelodysplastic Syndromes-Associated Gene Mutations Lead to Pseudohypoxia Condition and Epigenome Hyper-Methylation in Mouse Genetic Models
6. Mll-Partial Tandem Duplication (Mll-PTD) Causes Pseudohypoxia and Hypermethylation of the Epigenome through Suppression of Mitochondrial Complex II
7. Inducible Correction of a RUNX1 Mutation of Human AML Causes a Switch of AML to B-ALL
8. Myc Regulates the Development and Anti-Tumor Immunity of Natural Killer Cells
9. Essential Role of c-MYC for Natural Killer Cell Development, Proliferation and Anti-Tumor Activity
10. Activation of HIF Signaling in Mononuclear Phagocyte System Causes Hemophagocytic Lymphohistiocytosis in C57/BL6 Mice
11. Downregulation of SETD2-H3K36me3 Tumor Suppression Axis Promotes MLL Leukemia through Activation of DOT1L-H3K79me2 Axis
12. EPO Signaling Triggers Erythrocytosis By Expanding Erythrocytes and Also Subsets of Macrophages
13. SETD2, a H3K36 Lysine Methyltransferase, Is Essential for Adult Normal Hematopoiesis and Leukemia Stem Cells
14. HIF-1a Pathway, As a Signal Funnel for Genetic, Epigenetic, and Metabolic Aberrations, Is Sufficient and Essential for MDS Development
15. Two Novel Knock-in and Knock-out of Setd2 Alleles Cooperate with Mll-Af9 Knock-in Allele to Accelerate Leukemia Development
16. Activation of HIF-2a-EPO Axis in Kidney or Liver Is Sufficient to Drive Erythrocytosis in a Novel Inducible HIF-2a Transgenic Mouse Model
17. Global Crosstalk between Two Histone Modifications That Control Transcriptional Elongation in MLL Leukemia
18. Monotcytes/Macrophages Are Involved in Erythrocytosis Caused By Both EPO-Dependent and -Independent Activation of EPOR
19. RUNX1/CBFβ Dosage Is Critical for MLL Leukemias Development
20. Novel Myelodysplastic Syndromes-like Mouse Models By Cooperating Genetic/Epigenetic Mutations Reveal the Critical Role of HIF-1α for Disease Development
21. PU.1 Is Essential For MLL Leukemia Via Activation Of The Meis/HOX Pathway and A Monocytic Cytokine Mediated Anti-Apoptotic Inflammatory Program
22. Modeling and Targeting MLL-PTD/RUNX1 Related MDS/AML In Mouse
23. Modeling MLL-PTD Related Myelodysplastic Syndromes in Mouse.
24. Whole-Genome Sequencing of a Monozygotic Twin Pair Reveals Functional Cooperative Mutations of SETD2 in Acute Leukemia
25. The ability of MLL to bind RUNX1 and methylate H3K4 at PU.1 regulatory regions is impaired by MDS/AML-associated RUNX1/AML1 mutations
26. Essential Role for PU.1 in MEIS1 Activation and MLL Fusion Leukemia,
27. MLL-PTD Causes Hypomorph Condition of CBF Complex (RUNX1/CBFβ) and Predisposes the Abnormal Hematopoietic Stem and Progenitor Cells (HSPCs) to Clonal Expansion
28. Differential MLL Interaction and H3K4me3 Mark Maintenance at PU.1 Regulatory Region by AML Translocations-Associated Oncoproteins AML1-ETO and CBFβ-SMMHC.
29. Previously Unknown Interactions Between AML1 and MLL Provide Epigenetic Regulation of Gene Expression in Normal Hematopoiesis and in Leukemia
30. HIF1A Is a Critical Downstream Mediator for Hemophagocytic Lymphohistiocytosis
31. The High NRF2 Expression Confers Chemotherapy Resistance through Upregulated DUSP1 in Myelodysplastic Syndromes
32. Downregulation of SETD2-H3K36me3 Tumor Suppression Axis Promotes MLLLeukemia through Activation of DOT1L-H3K79me2 Axis
33. Essential Role for PU.1 in MEIS1Activation and MLL Fusion Leukemia,
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