Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Cell Biology, angiogenesis, cell cycle, endothelial cell, metabolism, quiescence, PROTEIN-KINASE ACTIVITY, PYRUVATE-KINASE, GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE, ENDOTHELIAL-CELLS, RESTRICTION POINT, TUMOR-GROWTH, HELA-CELLS, NOTCH, PROLIFERATION, ANGIOGENESIS, Adaptor Proteins, Signal Transducing, Animals, Calcium-Binding Proteins, Cell Cycle, Cell Cycle Proteins, Cell Proliferation, Cells, Cultured, Energy Metabolism, G1 Phase Cell Cycle Checkpoints, Glycolysis, Human Umbilical Vein Endothelial Cells, Humans, Intercellular Signaling Peptides and Proteins, Phenotype, Phosphofructokinase-2, Receptors, Notch, Signal Transduction, Transfection, Ubiquitin-Protein Ligases, 0601 Biochemistry and Cell Biology, Developmental Biology, 3101 Biochemistry and cell biology

Abstract:

Cell division is a metabolically demanding process, requiring the production of large amounts of energy and biomass. Not surprisingly therefore, a cell's decision to initiate division is co-determined by its metabolic status and the availability of nutrients. Emerging evidence reveals that metabolism is not only undergoing substantial changes during the cell cycle, but it is becoming equally clear that metabolism regulates cell cycle progression. Here, we overview the emerging role of those metabolic pathways that have been best characterized to change during or influence cell cycle progression. We then studied how Notch signaling, a key angiogenic pathway that inhibits endothelial cell (EC) proliferation, controls EC metabolism (glycolysis) during the cell cycle.