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Non-catalytic functions of Tet2 are essential to regulate hematopoietic stem and progenitor cell homeostasis
PubMed Full text in PMC Similar studies SRA Run Selector
Comparative analysis of Tet2 catalytic deficient and knockout bone marrow over time
PubMed Full text in PMC Similar studies
SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function
PubMed Full text in PMC Similar studies Analyze with GEO2R
SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [hMeDIP-Seq]
SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]
Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells
Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells [hME-Seal]
Tet2 loss dysregulates the behavior of bone marrow derived mesenchymal stromal cells [RNA-seq]
TET2 protects the genome from mutagenicity through interacting with MSH6
Epigenome analysis of patients with various myeloid malignancies including differential levels of 5-hydroxymethylcytosine
miRNA Expression Profiles in Human AML Samples And in Human and Mouse Blood Cell Lines
Restoration of genome-wide 5-hydroxymethylation by azacitidine and ascorbate in TET2-deficient human pre-leukemic HSPCs
Reduced representation bisulfite-sequencing of human leukemia cells and mouse hematopoietic progenitors
hMeDIP sequencing of human leukemia cells
Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia
RNA-sequencing of human leukemia cells and mouse hematopoietic progenitors
Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation
Effect of Tet2 loss in bone marrow progenitors
PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet
DNMT3A and TET2 Mutations Increase Hematopoietic Stem Cell Fitness Through Distinct Mechanisms
Expression data from Tet2-hypomorph (knockdown) and/or Ezh2-null Lineage-Sca-1+c-Kit+ (LSK) cells and granulocyte-macrophage progenitors (GMPs)
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