TIFAB modulates metabolic pathways in KMT2A::MLLT3−induced AML through HNF4A

Keyphrases

• Acute Myeloid Leukemia 100%
• Hepatocyte nuclear Factor 4α (HNF4α) 100%
• Metabolic Pathway 100%
• KMT2A 100%
• Leukemia 66%
• Leukemia Cells 33%
• HOXA9 33%
• Stem Progenitor Cells 33%
• NF-B 33%
• Cell Engraftment 33%
• Tumor Necrosis Factor-α 16%
• MTORC1 Signaling 16%
• Knockdown 16%
• Cell Function 16%
• Overexpressing 16%
• Metabolism 16%
• Glycolysis 16%
• Interacting Proteins 16%
• Tumorigenesis 16%
• Glucose Uptake 16%
• Nuclear Receptor 16%
• Metabolic Defects 16%
• Hematopoiesis 16%
• RelB 16%
• Oxidative Phosphorylation (OXPHOS) 16%
• Gene Set Enrichment Analysis 16%
• Mitochondrial Function 16%
• Novel Regulator 16%
• MEIS1 16%
• Uptake Function 16%
• Organ Development 16%
• P53 Pathway 16%
• Ubiquitin-specific Peptidase 16%
• Forkhead-associated Domain 16%
• Myelodysplastic Neoplasms 16%

Biochemistry, Genetics and Molecular Biology

• Myeloid 100%
• KMT2A 100%
• Hepatocyte Nuclear Factor 4 Alpha 75%
• Progenitor Cell 50%
• Downregulation 25%
• Tumor Necrosis Factor 25%
• Cell Function 25%
• Carcinogenesis 25%
• P53 25%
• Metabolic Pathway 25%
• Organogenesis 25%
• HOXA9 25%
• Glucose Transport 25%
• Ubiquitin 25%
• Hematopoiesis 25%
• Peptidase 25%
• Nuclear Receptor 25%
• Oxidative Phosphorylation 25%
• MEIS1 25%
• Forkhead-Associated Domain 25%
• Genome-Wide Analysis of Gene Expression 25%