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Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 09/2011, Volume 194, Issue 5, p. 751
The c-Jun N-terminal kinase (JNK) signaling pathway is essential for neuronal degeneration in multiple contexts but also regulates neuronal homeostasis. It... 
Signal transduction | Neurons | Kinases | Cells | Apoptosis
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 2/1998, Volume 140, Issue 4, pp. 911 - 923
To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring neuronal death, we examined neonatal sympathetic neurons that... 
Receptors | Phosphorylation | Neurons | Cell death | Nerves | Antibodies | Mice | Adulthood | PC12 cells | Apoptosis | PROGRAMMED CELL-DEATH | AFFINITY NGF RECEPTOR | TRK PROTOONCOGENE PRODUCT | GENE-EXPRESSION | DIFFERENTIATION | PC12 CELLS | C-JUN | BINDING | BRAIN | NERVE GROWTH-FACTOR | CELL BIOLOGY | Cell receptors | Analysis | Physiological aspects | Nervous system | Neurotropin | Degeneration
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2012, Volume 7, Issue 1, p. e30376
Caspase-6 is a cysteinyl protease implicated in neurodegenerative conditions including Alzheimer's and Huntington's disease making it an attractive target for... 
NEUROFIBRILLARY TANGLES | ALZHEIMER-DISEASE | APOPTOSIS | ACTIVATION | MULTIDISCIPLINARY SCIENCES | DEATH | INHIBITORS | HUNTINGTONS-DISEASE | SELECTIVITY | PEPTIDE | DEGENERATION | L-Lactate Dehydrogenase - metabolism | Caspase 6 - metabolism | Apoptosis - drug effects | Humans | Molecular Sequence Data | Cells - enzymology | Protease Inhibitors - pharmacology | Protein Isoforms - metabolism | Protein Processing, Post-Translational - drug effects | Cell Membrane - metabolism | Cell Membrane - drug effects | Recombinant Proteins - metabolism | Amino Acid Sequence | Cell Line | Cells - drug effects | Peptides - chemistry | Enzyme Assays - methods | Biological Assay - methods | Lamin Type A - metabolism | Enzyme Activation - drug effects | Caspase Inhibitors | Blotting, Western | Peptides - pharmacology | Animals | Substrate Specificity - drug effects | Mice | Staurosporine - pharmacology | Usage | Peptides | Proteases | Proteolysis | Amino acids | Drug discovery | Health aspects | Enzyme-linked immunosorbent assay | Neurosciences | Genomes | Assaying | Muscular dystrophy | Proteins | Clonal deletion | E coli | Deletion | Trends | Alzheimer's disease | Content analysis | Recombinant | Biodegradation | Enzymes | Neurodegenerative diseases | Caspase | Substrate inhibition | Lactate dehydrogenase | Pharmacology | Chemiluminescence | Peptide inhibitors | Huntington's disease | L-Lactate dehydrogenase | Caspase-6 | Inhibitors | Lactic acid | Mutation | Alzheimers disease | Apoptosis
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 12/1998, Volume 143, Issue 6, pp. 1691 - 1703
Naturally occurring sympathetic neuron death is the result of two apoptotic signaling events: one normally suppressed by NGF/TrkA survival signals, and a... 
Receptors | Neuroscience | Phosphorylation | Neurons | Cell death | Adenoviruses | Nerves | Antibodies | Viruses | Apoptosis | Nerve growth factor | Neuronal apoptosis | Brain-derived neurotrophic factor | MEKK | Sympathetic neurons | ACTIVATED PROTEIN-KINASE | PROTOONCOGENE PRODUCT | TYROSINE PHOSPHORYLATION | P53-DEPENDENT APOPTOSIS | sympathetic neurons | neuronal apoptosis | NERVE GROWTH-FACTOR | CELL BIOLOGY | PROGRAMMED CELL-DEATH | nerve growth factor | GENE-EXPRESSION | RAT SYMPATHETIC NEURONS | brain-derived neurotrophic factor | C-JUN | TRANSCRIPTION FACTOR | Receptor, trkA | Apoptosis - drug effects | Receptor Protein-Tyrosine Kinases - physiology | Receptors, Nerve Growth Factor - physiology | Neurons - cytology | Tumor Suppressor Protein p53 - genetics | Nerve Growth Factors - pharmacology | Superior Cervical Ganglion - physiology | Tumor Suppressor Protein p53 - physiology | Cell Death | Neurons - physiology | JNK Mitogen-Activated Protein Kinases | Nerve Growth Factors - physiology | Neurons - drug effects | Protein-Serine-Threonine Kinases - metabolism | Mitogen-Activated Protein Kinases | Proto-Oncogene Proteins - metabolism | Signal Transduction | Cells, Cultured | Rats | bcl-2-Associated X Protein | Superior Cervical Ganglion - cytology | Tumor Suppressor Protein p53 - deficiency | Receptor, Nerve Growth Factor | Mice, Knockout | Animals | Proto-Oncogene Proteins - physiology | Mice | Apoptosis - physiology | Models, Neurological | Proto-Oncogene Proteins c-bcl-2 | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | MAP Kinase Kinase Kinase 1 | Tumor suppressor genes | Genetic aspects | Neurotropin | Research
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 09/2013, Volume 202, Issue 5, p. 747
  Neurons are highly polarized cells that often project axons a considerable distance. To respond to axonal damage, neurons must transmit a retrograde signal... 
Signal transduction | Phosphorylation | Neurons | Stress response | Kinases | Apoptosis
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 09/2011, Volume 194, Issue 5, pp. 751 - 764
The c-Jun N-terminal kinase (JNK) signaling pathway is essential for neuronal degeneration in multiple contexts but also regulates neuronal homeostasis. It... 
PROGRAMMED CELL-DEATH | SIGNALING PATHWAY | N-TERMINAL KINASE | WALLERIAN DEGENERATION | SYMPATHETIC NEURONS | ACTIVATED PROTEIN-KINASES | C-JUN | MICROTUBULE DYNAMICS | MICE LACKING | NERVE GROWTH-FACTOR | CELL BIOLOGY | RNA, Small Interfering - genetics | Caspase 9 - metabolism | Central Nervous System - metabolism | Apoptosis - drug effects | Homeodomain Proteins - metabolism | Caspase 3 - metabolism | Central Nervous System - pathology | Axons - physiology | Ganglia, Spinal - cytology | Central Nervous System - embryology | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Protein Kinase Inhibitors - pharmacokinetics | Embryo, Mammalian - pathology | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Ganglia, Spinal - embryology | MAP Kinase Kinase Kinases - genetics | Mice, Transgenic | MAP Kinase Kinase Kinases - metabolism | Mice, Knockout | Central Nervous System - cytology | Embryo, Mammalian - embryology | Axons - pathology | Ganglia, Spinal - pathology | Nerve Growth Factor - deficiency | Mice | Protein Binding - physiology | Neurons - pathology | Phosphorylation | Spinal Cord - metabolism | JNK Mitogen-Activated Protein Kinases - metabolism | Protein Transport - physiology | Extracellular Signal-Regulated MAP Kinases - metabolism | MAP Kinase Kinase Kinases - deficiency | Spinal Cord - pathology | Neurons - drug effects | Proto-Oncogene Proteins c-jun - genetics | Cells, Cultured | Axons - metabolism | Nerve Growth Factor - pharmacology | Mice, Inbred Strains | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Spinal Cord - embryology | Animals | Proto-Oncogene Proteins c-jun - metabolism | Adaptor Proteins, Signal Transducing - genetics | Apoptosis - physiology | Adaptor Proteins, Signal Transducing - metabolism | Physiological aspects | Neurons | Apoptosis
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 09/2013, Volume 202, Issue 5, pp. 747 - 747
Neurons are highly polarized cells that often project axons a considerable distance. To respond to axonal damage, neurons must transmit a retrograde signal to... 
Abundance
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 2013, Volume 202, Issue 5, pp. 747 - 763
Journal Article
NATURE CHEMICAL BIOLOGY, ISSN 1552-4450, 07/2013, Volume 9, Issue 7, pp. 466 - 466
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2010, Volume 107, Issue 50, p. 21795
  Oligodendrocyte precursor cells (OPCs) are lineage-restricted progenitors generally limited in vivo to producing oligodendrocytes. Mechanisms controlling... 
Proteins | Chromatin | Rodents | Stem cells | Gene expression | Ribonucleic acid--RNA
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 01/2011, Volume 194, Issue 5, pp. 751 - 764
The c-Jun N-terminal kinase (JNK) signaling pathway is essential for neuronal degeneration in multiple contexts but also regulates neuronal homeostasis. It... 
Journal Article
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 10/2010, Volume 30, Issue 40, pp. 13367 - 13372
Oligodendrocyte precursor cells (OPCs) are generated from multiple progenitor domains in the telencephalon in developmental succession from ventral to dorsal.... 
Journal Article
Science Translational Medicine, ISSN 1946-6234, 08/2017, Volume 9, Issue 403, p. eaag0394
Journal Article