86 results on '"Blobel, Gerd A."'
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2. Molecular basis of polycomb group protein-mediated fetal hemoglobin repression
3. Identification and characterization of RBM12 as a novel regulator of fetal hemoglobin expression
4. Regulation of Fetal Hemoglobin Production in Adult Erythroid Cells By Protein Phosphatase 6C (PPP6C)
5. Mechanisms of Polycomb Group Protein-Mediated Fetal Hemoglobin Silencing
6. Examining the Role of Individual Baf Chromatin Remodeling Complex Components in Globin Gene Regulation
7. Let-7 Inhibits HIC2 to Control BCL11A Transcription and Hemoglobin Switching
8. Disrupting the adult globin promoter alleviates promoter competition and reactivates fetal globin gene expression
9. Protein Phosphatase 6C (PPP6C) Loss Significantly Raises Fetal Hemoglobin Levels and Reduces Cell Sickling
10. Regulation of Fetal Hemoglobin Expression By the VHL-HIF1α Oxygen Sensing System
11. Interrogating Post-Transcriptional Mechanisms of Fetal Hemoglobin Regulation
12. HIC2 Controls Developmental Hemoglobin Switching By Repressing BCL11A Transcription
13. Isolated Changes in Chromatin Accessibility and Enhancer-Promoter Contacts at the β-Globin Locus Distinguish Fetal Hemoglobin Producing F-Cells from a-Cells
14. ZNF410 Uniquely Activates the NuRD Component CHD4 to Silence Fetal Hemoglobin Expression
15. A β-Globin Locus-Intrinsic Epigenetic Mechanism Underlies Fetal Globin Production in F-Cells
16. Control of Fetal Hemoglobin Levels By NFI Transcription Factors
17. HRI depletion cooperates with pharmacologic inducers to elevate fetal hemoglobin and reduce sickle cell formation
18. The HRI-regulated transcription factor ATF4 activates BCL11A transcription to silence fetal hemoglobin expression
19. Understanding heterogeneity of fetal hemoglobin induction through comparative analysis of F and A erythroblasts
20. Interrogating RNA Binding Proteins as Novel Regulators of Fetal Hemoglobin Expression
21. Heme-Regulated Inhibitor (HRI) Activates Transcription Factor ATF4 to Promote BCL11A Transcription and Fetal Hemoglobin Silencing
22. Heme-Regulated Inhibitor (HRI) Depletion Cooperates with Pharmacologic Inducers to Strongly Elevate Fetal Hemoglobin and Reduce Sickle Cell Formation
23. Understanding Heterogeneity of Fetal Hemoglobin Induction through Comparative Analysis of Stage-Matched F- and a-Cells
24. The E3 ligase adaptor molecule SPOP regulates fetal hemoglobin levels in adult erythroid cells
25. Domain-Focused CRISPR-Cas9 Screen Identifies the E3 Ubiquitin Ligase Substrate Adaptor Protein SPOP as a Novel Repressor of Fetal Hemoglobin
26. Heme-Regulated Inhibitor (HRI) Loss and Pharmacologic Treatments Cooperate to Strongly Elevate Fetal Hemoglobin and Reduce Sickle Cell Formation
27. Charting a noncoding gene for γ-globin activation
28. Comparison of Fetal and Adult Erythroid Chromosomal Architectures Identifies a Novel Fetal Hemoglobin Regulatory Region
29. The BET Protein BRD2 Cooperates with CTCF to Enforce a Transcriptional Boundary in Erythroid Cells
30. Deep Mining of Natural Genetic Variation in Erythroid Cells Reveals New Insights about In Vivo Transcription Factor Binding and Chromatin Accessibility
31. Forced chromatin looping raises fetal hemoglobin in adult sickle cells to higher levels than pharmacologic inducers
32. A dynamic intron retention program in the mammalian megakaryocyte and erythrocyte lineages
33. Genome Editing Recreates Hereditary Persistence of Fetal Hemoglobin in Primary Human Erythroblasts
34. A Novel Regulatory Region of the p27 Locus Is Required for Normal Erythroid p27 Expression, and Produces a Long Noncoding RNA with No Detectable Function
35. A Hyperactive Transcriptional State Marks Genome Reactivation during Mitotic Exit
36. A Dynamic Intron Retention Program in the Mammalian Megakaryocyte and Erythrocyte Lineages
37. Functions of BET proteins in erythroid gene expression
38. Epigenetics of Cellular Memory: Insights from the Chromatin Accessibility Landscape of the Mitotic Genome
39. Comparing Strategies to Reactivate Fetal Globin Expression for the Treatment of Beta-Globinopathies
40. Mechanistic Insights into Forced Chromatin Looping Mediated Activation of Fetal Globin Gene Expression
41. Dissection of BET Protein Function in a Hematopoietic Differentiation Model
42. Hematopoietic Transcriptional Regulation At The Mitosis-G1 Transition
43. Analysis of disease-causing GATA1 mutations in murine gene complementation systems
44. Controlling Long-Range Genomic Interactions to Reprogram the β-Globin Locus
45. GATA1 and the BET Family Protein Brd3 Form a Mitotic Bookmarking Complex
46. Dissecting the Molecular Pathways That Underlie Disease-Causing GATA1 Mutations
47. Pleiotropic platelet defects in mice with disrupted FOG1-NuRD interaction
48. Linking Transcription Factor Pathways to Disease-Causing GATA1 Mutations
49. Lineage-Specific Mitotic Bookmarking by Hematopoietic Transcription Factor GATA1
50. Acetylation-Dependent Interaction of GATA-1 with the Potential Mitotic “Bookmarking” Protein Brd3.
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