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Biochemical Journal, ISSN 0264-6021, 01/2010, Volume 425, Issue 1, pp. 215 - 223
The transcription factor SREBP1c (sterol-regulatory-element-binding protein 1c) is highly expressed in adipose tissue and plays a central role in several... 
Adipocyte | CCAAT/enhancer-binding protein(C/EBP) | Sterol-regulatory-element-binding protein 1c(SREBP1c) | Transcription | Lipid | Adipogenesis | transcription | BIOCHEMISTRY & MOLECULAR BIOLOGY | ELEMENT-BINDING PROTEIN-1C | ALPHA | sterol-regulatory-element-binding protein 1c (SREBP1c) | lipid | BETA | adipogenesis | INSULIN-RESISTANCE | adipocyte | LIPODYSTROPHY | ADIPOCYTE DIFFERENTIATION | PPAR-GAMMA | ADD1/SREBP1 | CCAAT/enhancer-binding protein (C/EBP) | MICE | ADIPOSE-TISSUE | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Humans | Adipocytes - cytology | DNA-Binding Proteins - metabolism | Chromatin Immunoprecipitation | RNA Interference | CCAAT-Enhancer-Binding Protein-delta - metabolism | CCAAT-Enhancer-Binding Proteins - genetics | Sterol Regulatory Element Binding Protein 1 - metabolism | CCAAT-Enhancer-Binding Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Promoter Regions, Genetic | CCAAT-Enhancer-Binding Protein-beta - genetics | Cells, Cultured | Gene Expression Regulation | Proto-Oncogene Proteins - genetics | Transcription Factors - genetics | 3T3-L1 Cells | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | CCAAT-Enhancer-Binding Protein-beta - metabolism | RUNX1 Translocation Partner 1 Protein | Transcription Factors - metabolism | Animals | Sterol Regulatory Element Binding Protein 1 - genetics | CCAAT-Enhancer-Binding Protein-delta - genetics | Adipocytes - metabolism | CCAAT-Enhancer-Binding Protein-alpha - genetics | Protein Binding | Mice | Index Medicus
Journal Article
PLoS Genetics, ISSN 1553-7390, 07/2017, Volume 13, Issue 7, pp. e1006887 - e1006887
MicroRNA cluster mirn23a has previously been shown to promote myeloid development at the expense of lymphoid development in overexpression and knockout mouse... 
Guanylate Kinases - genetics | NIH 3T3 Cells | Up-Regulation | Cell Proliferation | MicroRNAs - metabolism | Mitochondrial Proteins - genetics | Phosphatidylinositol 3-Kinases - metabolism | Mitochondrial Proteins - metabolism | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Cell Differentiation | Membrane Proteins - metabolism | B-Lymphocytes - metabolism | Cell Line | Forkhead Box Protein O1 - metabolism | Promoter Regions, Genetic | Signal Transduction | Membrane Proteins - genetics | Down-Regulation | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Hematopoiesis - genetics | Phosphatidylinositol 3-Kinases - genetics | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Guanylate Kinases - metabolism | Trans-Activators - metabolism | Mice | MicroRNAs - genetics | Forkhead Box Protein O1 - genetics | Apoptosis | RNA sequencing | MicroRNA | Hematopoiesis | Physiological aspects | Genetic aspects | Genetic transcription | Observations | Methods | Cell culture | Flow cytometry | Polarization | Visualization | Smad protein | Animal models | Transcription factors | Gene regulation | AKT protein | In vitro testing | Kinases | Pax5 protein | Proteins | Signal transduction | Immunology | Pathways | FOXO1 protein | Bone marrow | Clusters | Bone morphogenetic proteins | Buffers | Research centers | Medical research | MiRNA | Transplants | Cell lineage | Runx1 protein | Pharmacology | 1-Phosphatidylinositol 3-kinase | Hemopoiesis | Cytometry | Inhibitors | Ribonucleic acids | Lymphocytes B | MicroRNAs | Stem cells | In vivo methods and tests | Differentiation | Cancer | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2016, Volume 291, Issue 9, pp. 4732 - 4741
AML1-ETO is the most common fusion oncoprotein causing acute myeloid leukemia (AML), a disease with a 5-year survival rate of only 24%. AML1-ETO functions as a... 
COMPLEX | DOMAIN | CCT | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | INTRANUCLEAR MOBILITY | ACUTE MYELOID-LEUKEMIA | EUKARYOTIC CHAPERONIN | CYTOPLASMIC CHAPERONIN | PROTEINS | TRANSCRIPTION FACTOR | Protein Subunits | Oncogene Proteins, Fusion - metabolism | Immunoprecipitation | Humans | Gene Expression Regulation, Neoplastic | Neoplasm Proteins - antagonists & inhibitors | Neoplasm Proteins - metabolism | Recombinant Fusion Proteins - metabolism | Oncogene Proteins, Fusion - chemistry | Core Binding Factor Alpha 2 Subunit - chemistry | Cattle | HEK293 Cells | Protein Interaction Domains and Motifs | Protein Stability | Chaperonin Containing TCP-1 - metabolism | Peptide Fragments - genetics | Peptide Fragments - metabolism | Core Binding Factor Alpha 2 Subunit - metabolism | Cell Survival | Models, Molecular | Rats | Neoplasm Proteins - chemistry | Recombinant Fusion Proteins - chemistry | Reticulocytes - metabolism | Protein Folding | HSP70 Heat-Shock Proteins - metabolism | RUNX1 Translocation Partner 1 Protein | Peptide Fragments - chemistry | Animals | Chaperonin Containing TCP-1 - antagonists & inhibitors | Oncogene Proteins, Fusion - genetics | Protein Conformation | Chaperonin Containing TCP-1 - chemistry | Core Binding Factor Alpha 2 Subunit - genetics | Index Medicus | AML1-ETO | Protein Structure and Folding | leukemia | fusion protein | chaperone | chaperonin | protein folding | TRiC
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 7, pp. 1 - 18
Background: Notch receptor signaling controls developmental cell fates in a cell-context dependent manner. Although Notch signaling directly regulates... 
PROGENITOR CELLS | SKELETAL-MUSCLE | STEM-CELLS | RBP-J-KAPPA | MOUSE EMBRYOGENESIS | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | DOWN-REGULATION | FATE | EXPRESSION | Paired Box Transcription Factors - genetics | Cell Cycle - genetics | Embryonic Stem Cells - metabolism | Embryonic Stem Cells - cytology | Oligonucleotide Array Sequence Analysis | Myogenic Regulatory Factor 5 - genetics | Homeodomain Proteins - metabolism | Apoptosis - genetics | DNA-Binding Proteins - metabolism | Cell Differentiation - genetics | Myogenic Regulatory Factor 5 - metabolism | Eye Proteins - genetics | Cell Differentiation - physiology | Repressor Proteins - metabolism | SOX9 Transcription Factor - metabolism | Cell Line | Core Binding Factor Alpha 2 Subunit - metabolism | Repressor Proteins - genetics | PAX6 Transcription Factor | Receptor, Notch1 - metabolism | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Homeodomain Proteins - genetics | Animals | Eye Proteins - metabolism | Cell Cycle - physiology | Mice | Apoptosis - physiology | Receptor, Notch1 - genetics | Core Binding Factor Alpha 2 Subunit - genetics | SOX9 Transcription Factor - genetics | Paired Box Transcription Factors - metabolism | Analysis | Genes | Genetic research | Protein biosynthesis | Genetic transcription | DNA binding proteins | Tamoxifen | Cell differentiation | Embryonic stem cells | Protein binding | Transcription factors | Ontology | Sox9 protein | Genomics | Differentiation (biology) | Embryo cells | Decisions | Stem cell transplantation | Smooth muscle | Genomes | Biology | Biochemistry | Tissues | Proteins | Consortia | Allografts | Cell fate | Repressors | Cell cycle | Bioinformatics | Deoxyribonucleic acid--DNA | Biomedical engineering | Data analysis | Dendritic cells | Runx1 protein | Mammals | Gene expression | Signalling | Studies | Pax6 protein | Musculoskeletal system | Protein synthesis | Collaboration | Stem cells | Ligands | Notch protein | Binding sites | Apoptosis | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Molecular Cell, ISSN 1097-2765, 02/2012, Volume 45, Issue 3, pp. 330 - 343
Polycomb repressive complexes (PRCs) play key roles in developmental epigenetic regulation. Yet the mechanisms that target PRCs to specific loci in mammalian... 
TRANSFORMATION | MAINTENANCE | ADULT HEMATOPOIESIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEMATOPOIETIC STEM-CELLS | CBFA2 | MEGAKARYOCYTE | MICE | DIFFERENTIATION | RUNX1 | HAPLOINSUFFICIENCY | CELL BIOLOGY | Chromatin - metabolism | Thymocytes - metabolism | Protein Multimerization | Gene Expression Profiling | Core Binding Factor beta Subunit - genetics | Zebrafish - embryology | Gene Knockdown Techniques | T-Lymphocytes - metabolism | Hematopoietic Stem Cells - physiology | Repressor Proteins - isolation & purification | Megakaryocytes - metabolism | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Core Binding Factor beta Subunit - metabolism | Proto-Oncogene Proteins - metabolism | Cell Line | Core Binding Factor Alpha 2 Subunit - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Ubiquitin-Protein Ligases - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Polycomb-Group Proteins | Zebrafish - genetics | Mice, Knockout | Animals | Chromatography, Affinity | Polycomb Repressive Complex 1 | Protein Binding | Mice | Ubiquitin-Protein Ligases - genetics | Core Binding Factor Alpha 2 Subunit - genetics | Cluster Analysis | Computer science | Employee recruitment | Chromatin | Genomics | Genes | Stem cells | Chemical properties | DNA binding proteins | Artificial intelligence | Genetic research | Index Medicus
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 10/2001, Volume 21, Issue 19, pp. 6470 - 6483
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
NUCLEAR RECEPTOR COREPRESSORS | PROMYELOCYTIC LEUKEMIA | GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | N-COR | TRANSCRIPTIONAL REPRESSION | FUSION PROTEIN | CLASS-I | GRANULOCYTIC DIFFERENTIATION | CELL-CYCLE | ACUTE MYELOID-LEUKEMIA | CELL BIOLOGY | Translocation, Genetic | Transcription Factors - chemistry | Nuclear Receptor Co-Repressor 1 | Molecular Sequence Data | DNA-Binding Proteins - metabolism | Oncogene Proteins, Fusion - physiology | Core Binding Factor Alpha 2 Subunit | Transcription, Genetic | Proto-Oncogene Proteins | Binding Sites | Hydroxamic Acids - pharmacology | Repressor Proteins - metabolism | Protein Structure, Tertiary | Amino Acid Sequence | Cell Line | DNA-Binding Proteins - physiology | Leukemia, Myelomonocytic, Acute - genetics | Transcription Factors - physiology | Enzyme Inhibitors - pharmacology | Histone Deacetylases - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | DNA-Binding Proteins - chemistry | RUNX1 Translocation Partner 1 Protein | Sequence Homology, Amino Acid | Transcription Factors - metabolism | Animals | Oncogene Proteins, Fusion - antagonists & inhibitors | Histone Deacetylase Inhibitors | Mice | Models, Genetic | Nuclear Proteins - physiology | AML-1 protein | HDAC-2 protein | N-CoR protein | ETO protein | trichostatin A | chromosome 21 | mSin3A protein | chromosome 8 | histone deacetylase | HDAC-3 protein | Index Medicus | Transcriptional Regulation
Journal Article
Nature Cell Biology, ISSN 1465-7392, 07/2017, Volume 19, Issue 7, pp. 844 - 855
Leukaemogenesis requires enhanced self-renewal, which is induced by oncogenes. The underlying molecular mechanisms remain incompletely understood. Here, we... 
RIBOSOMAL-RNA METHYLATION | BREAST-CANCER | BIOGENESIS | HEMATOPOIETIC STEM-CELLS | TRANSCRIPTION | GRANULOCYTIC DIFFERENTIATION | ACUTE MYELOID-LEUKEMIA | PROTEIN-SYNTHESIS | POLYMERASE-I | TRANSLATIONAL CONTROL | CELL BIOLOGY | Myeloid-Lymphoid Leukemia Protein - metabolism | Oncogene Proteins, Fusion - metabolism | Cell Proliferation | Leukemia - pathology | Humans | Leukemia - metabolism | RNA, Ribosomal - genetics | Protein Interaction Maps | Cell Self Renewal | RNA, Small Nucleolar - metabolism | Time Factors | Cell Transformation, Neoplastic - genetics | U937 Cells | HEK293 Cells | Ribonucleoproteins - genetics | DEAD-box RNA Helicases - metabolism | Leukemia - genetics | Repressor Proteins - metabolism | Genetic Predisposition to Disease | Core Binding Factor Alpha 2 Subunit - metabolism | Signal Transduction | Mice, Inbred C57BL | RNA, Ribosomal - metabolism | Repressor Proteins - genetics | Ribonucleoproteins - metabolism | Gene Expression Regulation, Leukemic | Transcription Factors - genetics | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | RNA, Small Nucleolar - genetics | Mice, Knockout | RUNX1 Translocation Partner 1 Protein | Transcription Factors - metabolism | DEAD-box RNA Helicases - genetics | Phenotype | Animals | Myeloid-Lymphoid Leukemia Protein - genetics | Oncogene Proteins, Fusion - genetics | K562 Cells | HL-60 Cells | Proto-Oncogene Proteins c-myc - genetics | Cell Transformation, Neoplastic - pathology | Methylation | Core Binding Factor Alpha 2 Subunit - genetics | Enhancer-of-split protein | Leukemia | rRNA | Myc protein | snoRNA | DNA helicase | AML1 protein | Molecular modelling | Clonal deletion | Ribonucleic acids | Stem cells | Deletion | In vitro methods and tests | RNA helicase | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, pp. e0126385 - e0126385
The murine Cebpa gene contains an evolutionarily conserved 453 bp enhancer located at +37 kb that, together with its promoter, directs expression to myeloid... 
CELLS | INHIBITION | MULTIDISCIPLINARY SCIENCES | GRANULOCYTIC DIFFERENTIATION | C-MYB | LEUKEMIA | PROMOTER | TRANSCRIPTION FACTOR | CCAAT-Enhancer-Binding Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Cell Line | CCAAT-Enhancer-Binding Protein-alpha - metabolism | Core Binding Factor Alpha 2 Subunit - metabolism | Proto-Oncogene Proteins c-ets - genetics | Humans | Proto-Oncogene Proteins - genetics | Regulatory Sequences, Nucleic Acid - genetics | Point Mutation - genetics | Animals | GATA2 Transcription Factor - metabolism | Trans-Activators - genetics | CCAAT-Enhancer-Binding Protein-alpha - genetics | Protein Binding | Trans-Activators - metabolism | Enhancer Elements, Genetic - genetics | Mice | Proto-Oncogene Proteins c-ets - metabolism | CCAAT-Enhancer-Binding Proteins - genetics | Core Binding Factor Alpha 2 Subunit - genetics | GATA2 Transcription Factor - genetics | Pediatrics | Transformation | Transcription factors | Ets-1 protein | Transcription | Leukemia | Stem cell transplantation | Oncology | Genomes | CCAAT/enhancer-binding protein | CEBPA gene | FLI-1 protein | Hematopoietic stem cells | PU.1 protein | Allografts | Granulocytes | Granulocyte colony-stimulating factor | Interleukin 3 | Hematopoiesis | Rodents | c-Myb protein | Deoxyribonucleic acid--DNA | CRISPR | Myeloid cells | Myeloid leukemia | Transgenic mice | Runx1 protein | Gene expression | Monocytes | Stem cells | Genetic engineering | Mutation | Leukocytes (granulocytic) | Acute myeloid leukemia | Integrity | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Science, ISSN 0036-8075, 8/2011, Volume 333, Issue 6043, pp. 765 - 769
The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional... 
Cell growth | Myeloid leukemia | Leukemia | Genes | REPORTS | Antibodies | Histones | Amino acids | Acetylation | Leukocytes | Cells | DNA-BINDING | DOMAIN | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | T(8/21) | TRANSCRIPTION | FUSION PROTEIN | MYELOID-LEUKEMIA | SELF-RENEWAL | DIFFERENTIATION | INHIBITOR | Oncogene Proteins, Fusion - metabolism | Humans | Leukemia, Myeloid, Acute - metabolism | Transcriptional Activation | Preleukemia - pathology | E1A-Associated p300 Protein - metabolism | Gene Expression Profiling | Oncogene Proteins, Fusion - chemistry | Core Binding Factor Alpha 2 Subunit - chemistry | E1A-Associated p300 Protein - antagonists & inhibitors | Hematopoietic Stem Cells - physiology | Lysine - metabolism | Protein Interaction Domains and Motifs | Tumor Cells, Cultured | Cell Line | Core Binding Factor Alpha 2 Subunit - metabolism | Leukemia, Myeloid, Acute - pathology | Mice, Inbred C57BL | Mutant Proteins - metabolism | Fetal Blood - cytology | RUNX1 Translocation Partner 1 Protein | Preleukemia - metabolism | Animals | Cell Transformation, Neoplastic | Hematopoietic Stem Cells - cytology | Cell Line, Tumor | Protein Binding | Mice | Protein Processing, Post-Translational | Genetic aspects | Research | Lysine | Health aspects | Cancer cells | Proteins | Biochemistry | Cellular biology | Chromosomes | Rope | Mathematical models | Transformations | Leukemias | Blood | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, pp. e55481 - e55481
AML1-ETO fusion protein (AE) is generated by t(8;21)(q22;q22) chromosomal translocation, which is one of the most frequently observed structural abnormalities... 
AML1-ETO | PATHWAYS | MONOCYTIC LEUKEMIA | MULTIDISCIPLINARY SCIENCES | G1/S TRANSITION | AML1/ETO | TRANSCRIPTION | KINASE | FUSION PROTEIN | CBP/P300 | ACUTE MYELOID-LEUKEMIA | Oncogene Proteins, Fusion - metabolism | p300-CBP Transcription Factors - antagonists & inhibitors | Apoptosis - drug effects | Humans | Leukemia, Myeloid, Acute - metabolism | Proto-Oncogene Proteins c-kit - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | p300-CBP Transcription Factors - genetics | Leukemia, Myeloid, Acute - drug therapy | Female | Proto-Oncogene Proteins c-kit - genetics | Hematopoietic Stem Cells - drug effects | Core Binding Factor Alpha 2 Subunit - metabolism | Leukemia, Myeloid, Acute - pathology | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Gene Expression Regulation, Leukemic - drug effects | Hematopoietic Stem Cells - metabolism | RUNX1 Translocation Partner 1 Protein | Granulocyte Colony-Stimulating Factor - pharmacology | p300-CBP Transcription Factors - metabolism | Acetylation - drug effects | Animals | Histones - genetics | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Oncogene Proteins, Fusion - genetics | Hematopoietic Stem Cells - cytology | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Histones - metabolism | Core Binding Factor Alpha 2 Subunit - genetics | Proto-Oncogene Proteins c-bcl-2 - genetics | Leukemia, Myeloid, Acute - genetics | Physiological aspects | Genetic aspects | Research | Transferases | Cell proliferation | Transcription | Bcl-2 protein | Leukemia | Event-related potentials | Kinases | Proteins | Cell growth | Allografts | Granulocyte colony-stimulating factor | Peripheral blood | Cell cycle | Colony-stimulating factor | Inhibition | Acetylation | Fusion protein | G1 phase | Translocation | Hematology | Colonies | Myeloid leukemia | Abnormalities | Melanoma | Gene expression | Histone acetyltransferase | c-Kit protein | Patients | AML1 protein | Inhibitors | Cell lines | Stem cells | Leukemogenesis | Leukocytes (granulocytic) | Laboratory animals | Acute myeloid leukemia | Prostate cancer | Histone H3 | Apoptosis | Index Medicus
Journal Article
Journal Article