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Molecular Cell, ISSN 1097-2765, 05/2016, Volume 62, Issue 4, pp. 491 - 506
ULK1 and ULK2 are thought to be essential for initiating autophagy, and -deficient mice die perinatally of autophagy-related defects. Therefore, we used a... 
SEROTONIN TRANSPORTER | BIOGENESIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | EXIT SITES | EXPORT | NEURONS | AUTOPHAGOSOME FORMATION | ULK1 | COMPONENT | HOMOLOG | PROTEINS | CELL BIOLOGY | Golgi Apparatus - enzymology | Protein-Serine-Threonine Kinases - deficiency | Fibroblasts - enzymology | Phosphorylation | Vesicular Transport Proteins - metabolism | Autophagy-Related Protein 7 - metabolism | Humans | Brain - enzymology | Caenorhabditis elegans Proteins - metabolism | Homeostasis | Male | Autophagy-Related Protein-1 Homolog - metabolism | Golgi Apparatus - pathology | Mice, 129 Strain | Autophagy | Endoplasmic Reticulum - pathology | Transfection | RNA Interference | Time Factors | HEK293 Cells | Female | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Endoplasmic Reticulum - enzymology | Caenorhabditis elegans - genetics | Mice, Inbred C57BL | Vesicular Transport Proteins - genetics | Protein-Serine-Threonine Kinases - genetics | Genotype | Nuclear Proteins - metabolism | Unfolded Protein Response | Autophagy-Related Protein 7 - genetics | Mice, Knockout | Protein Transport | Carrier Proteins - genetics | Phenotype | Animals | Autophagy-Related Protein-1 Homolog - deficiency | COP-Coated Vesicles - enzymology | Carrier Proteins - metabolism | Brain - pathology | Nerve Degeneration | Autophagy-Related Protein-1 Homolog - genetics | Caenorhabditis elegans - enzymology | Proteins | Neurons | Phosphoproteins | Cells
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 02/2017, Volume 24, Issue 2, pp. 212 - 224
Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are of great importance in different cell contexts. However, only a very small number of... 
PLAYER | EVOLUTION | LONG NONCODING RNAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | ALPHA | PLURIPOTENCY | MECHANISMS | EXPRESSION | ACUTE PROMYELOCYTIC LEUKEMIA | CANCER BIOLOGY | CELL BIOLOGY | Oncogene Proteins, Fusion - metabolism | Leukemia, Promyelocytic, Acute - pathology | MicroRNAs - antagonists & inhibitors | Humans | Child, Preschool | Infant | Male | MicroRNAs - metabolism | Autophagy-Related Protein-1 Homolog - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Autophagy - drug effects | Proteolysis - drug effects | Leukemia, Promyelocytic, Acute - metabolism | HEK293 Cells | Female | E2F1 Transcription Factor - antagonists & inhibitors | Membrane Proteins - metabolism | Child | Intracellular Signaling Peptides and Proteins - genetics | Infant, Newborn | Tretinoin - pharmacology | Argonaute Proteins - metabolism | Argonaute Proteins - genetics | Membrane Proteins - genetics | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | E2F1 Transcription Factor - metabolism | Down-Regulation - drug effects | Mice, SCID | Animals | Membrane Proteins - antagonists & inhibitors | Cell Differentiation - drug effects | Oncogene Proteins, Fusion - genetics | Adolescent | Cell Line, Tumor | Oncogene Proteins, Fusion - antagonists & inhibitors | Mice | MicroRNAs - genetics | Leukemia, Promyelocytic, Acute - genetics | E2F1 Transcription Factor - genetics | Autophagy-Related Protein-1 Homolog - genetics | Autophagy-Related Protein-1 Homolog - antagonists & inhibitors | Original Paper
Journal Article
Journal Article
Cell Reports, ISSN 2211-1247, 10/2017, Volume 21, Issue 1, pp. 1 - 9
Reactive oxygen species (ROS) are continuously produced as a by-product of mitochondrial metabolism and eliminated via antioxidant systems. Regulation of... 
senescence | mitochondria | ROS | AMPK | PGC-1α | ULK1 | LKB1 | oxidative stress | nutrient signaling energy stress | CANCER-CELLS | SURVIVAL | COMPLEX-III | ENERGY STRESS | ACTIVATED PROTEIN-KINASE | GROWTH | NEURODEGENERATION | HYDROGEN-PEROXIDE | DIRECT PHOSPHORYLATION | CELL BIOLOGY | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics | Superoxide Dismutase - genetics | Reactive Oxygen Species - metabolism | Uncoupling Protein 3 - genetics | Humans | Autophagy-Related Protein-1 Homolog - metabolism | AMP-Activated Protein Kinases - deficiency | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - deficiency | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Superoxide Dismutase-1 - metabolism | HEK293 Cells | Protein Stability | Superoxide Dismutase - metabolism | Fibroblasts - metabolism | Cellular Senescence - genetics | Glutathione Peroxidase - metabolism | Uncoupling Protein 3 - metabolism | Signal Transduction | Uncoupling Protein 2 - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Gene Expression Regulation | Mice, Transgenic | Mitochondria - metabolism | Glutathione Peroxidase - genetics | Uncoupling Protein 2 - genetics | Metabolic Networks and Pathways - genetics | Animals | Superoxide Dismutase-1 - genetics | Fibroblasts - cytology | Mice | Primary Cell Culture | Autophagy-Related Protein-1 Homolog - genetics | AMP-Activated Protein Kinases - genetics | Homeostasis - genetics
Journal Article
Molecular Cell, ISSN 1097-2765, 05/2016, Volume 62, Issue 3, pp. 359 - 370
Metabolic reprogramming is fundamental to biological homeostasis, enabling cells to adjust metabolic routes after sensing altered availability of fuels and... 
GLYCOLYSIS | PENTOSE-PHOSPHATE PATHWAY | PROTEIN | INHIBITION | GLUCONEOGENESIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISEASE | GROWTH | FIP200 | FRUCTOSE-1,6-BISPHOSPHATASE | DIRECT PHOSPHORYLATION | CELL BIOLOGY | Protein-Serine-Threonine Kinases - deficiency | Phosphorylation | Reactive Oxygen Species - metabolism | Humans | Stress, Physiological | Male | Phosphopyruvate Hydratase - metabolism | Autophagy-Related Protein-1 Homolog - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Autophagy | DNA-Binding Proteins - metabolism | Amino Acids - metabolism | Transfection | MCF-7 Cells | RNA Interference | Time Factors | Cell Death | Biomarkers, Tumor - metabolism | Female | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | Signal Transduction | HCT116 Cells | Protein-Serine-Threonine Kinases - genetics | Genotype | Amino Acids - deficiency | Mice, Knockout | Fructose-Bisphosphatase - metabolism | Phenotype | Animals | Autophagy-Related Protein-1 Homolog - deficiency | Glucose - metabolism | Glycolysis | Hexokinase - metabolism | Phosphofructokinase-1 - metabolism | Autophagy-Related Protein-1 Homolog - genetics | Pentose Phosphate Pathway | Phosphates | Glucose metabolism | Enzymes | Medical colleges | Genetically modified organisms | Amino acids | Genetic engineering | Glucose | Fructose | Dextrose
Journal Article
Developmental Cell, ISSN 1534-5807, 10/2016, Volume 39, Issue 1, pp. 13 - 27
Journal Article
Scientific Reports, ISSN 2045-2322, 02/2016, Volume 6, Issue 1, p. 21772
Journal Article
Molecular Cell, ISSN 1097-2765, 09/2017, Volume 67, Issue 6, pp. 974 - 989.e6
Journal Article
Journal Article