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Biochemical journal, ISSN 1470-8728, 2010, Volume 427, Issue 1, pp. 69 - 78
More than 200 phosphorylated 14-3-3-binding sites in the literature were analysed to define 14-3-3 specificities, identify relevant protein kinases, and give insights into how cellular 14-3-3... 
Evolution | 14-3-3 protein | Disrupted-in-schizophrenia 1 (DISC1) | calmodulin-dependent protein kinase | AGC protein kinase | Ca | NEURONAL MIGRATION | SIGNALING PATHWAYS | MEMBRANE H+-ATPASE | REGULATING 14-3-3 BINDING | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | EUKARYOTIC PROTEIN-KINASES | evolution | NUCLEAR-LOCALIZATION | EXOENZYME-S | STRUCTURAL BASIS | Ca2+/calmodulin-dependent protein kinase | disrupted-in-schizophrenia 1 (DISC1) | ENDOPLASMIC-RETICULUM | Protein Kinases - metabolism | Phosphorylation | Immunoprecipitation | Humans | RNA, Messenger - genetics | Cells, Cultured | Computational Biology | Kidney - cytology | RNA, Messenger - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | 14-3-3 Proteins - metabolism | Nerve Tissue Proteins - metabolism | Kidney - metabolism | Carrier Proteins - metabolism | Protein Binding | Binding Sites | Dimerization | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | 14-3-3 Proteins - genetics | Bcl-2-associated death promoter | AANAT, serotonin acetyltransferase | FOXO, Forkhead box O | KLC, kinesin light chain | CDK5, cyclin-dependent kinase 5 | HEK, human embryonic kidney | MARK, microtubule affinity-regulating kinase | AMPK, AMP-activated protein kinase | EST, expressed sequence tag | PKB, protein kinase B | RSK, ribosomal S6 kinase | CaMK, Ca2 | GLUT4, glucose transporter 4 | protein kinase G | GST, glutathione transferase | HDAC, histone deacetylase | HAP1A, Huntingtin-associated protein 1A | DIG, digoxigenin | PKC, protein kinase C | BAD, Bcl-XL | PP2A, protein phosphatase 2A | DSTT, Division of Signal Transduction Therapy | HA, haemagglutinin | AGC, protein kinase A | Ca2 | PI4K, phosphoinositide 4-kinase | DISC1, disrupted-in-schizophrenia 1 | protein kinase C family kinase | YAP1, yes-associated protein 1
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, p. e95914
Protein conformational maladies such as Huntington Disease are characterized by accumulation of intracellular and extracellular protein inclusions containing amyloid-like proteins... 
NEURONAL INTRANUCLEAR INCLUSIONS | EXPANDED POLYGLUTAMINE | UBIQUITIN-PROTEASOME SYSTEM | EXPANSION PROTEINS | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | MUTANT HUNTINGTIN | CASPASE CLEAVAGE | BODY FORMATION | SACCHAROMYCES-CEREVISIAE | TRANSCRIPTION FACTOR | Protein Aggregates | RNA-Binding Proteins - genetics | Ribonucleases - genetics | Saccharomyces cerevisiae - genetics | Humans | Huntington Disease - pathology | Molecular Sequence Data | Amyloidogenic Proteins - chemistry | Intracellular Signaling Peptides and Proteins - metabolism | Ribonucleases - metabolism | Saccharomyces cerevisiae - metabolism | Heat-Shock Proteins - genetics | Nerve Tissue Proteins - chemistry | Peptides - metabolism | Nuclear Proteins - deficiency | Nuclear Proteins - genetics | Transgenes | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Amyloidogenic Proteins - genetics | Gene Expression Regulation, Fungal | Protein Structure, Tertiary | Amino Acid Sequence | Peptides - chemistry | Signal Transduction | Heat-Shock Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | HSP70 Heat-Shock Proteins - genetics | Saccharomyces cerevisiae Proteins - genetics | Nuclear Localization Signals | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | HSP70 Heat-Shock Proteins - metabolism | Protein Interaction Mapping | Nerve Tissue Proteins - metabolism | Huntingtin Protein | Amyloidogenic Proteins - metabolism | Models, Biological | Plasmids | Saccharomyces cerevisiae Proteins - metabolism | Huntington Disease - genetics | Protein Binding | Proteins | Proline | Heat shock proteins | Huntington's chorea | Quality control | Transcription factors | Disease | Huntingtin | Toxicity | Cytotoxicity | Biology | Agglomeration | Defense mechanisms | Nuclei | Cell cycle | Physiology | Localization | RNA processing | Trinucleotide repeat diseases | Polyglutamine | Benign | Hsp70 protein | Gene expression | Ribonucleic acid--RNA | Disease control | Suppressors | Intermediates | Prions | Intracellular | Protein interaction | Cytoplasm | RNA | Ribonucleic acid
Journal Article
FEBS Letters, ISSN 0014-5793, 07/2015, Volume 589, Issue 16, pp. 2100 - 2109
... protein aggregates [2] . Since autophagy contributes to cell growth, adaptation, and differentiation, its malfunction is intimately associated with human diseases [3... 
Screening | G6PT | ULK1 | ATG9 | Autophagy modulator | glucose-6-phosphate transporter | N-terminus of Venus vector | chlorogenic acid | BiFC | bimolecular fluorescence complementation | CHA | C-terminus of Venus vector | NEURODEGENERATIVE DISEASE | DISEASE TYPE-IB | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-GROWTH | MACROAUTOPHAGY | MTOR | CELL BIOLOGY | MAMMALIAN ATG PROTEINS | FORMATION SITE | BIOPHYSICS | SIGNALING PATHWAY | AMINO-ACIDS | ANTIPORTER DEFICIENT | Up-Regulation | TOR Serine-Threonine Kinases - metabolism | Vesicular Transport Proteins - metabolism | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Multiprotein Complexes - metabolism | RNA Interference | Intracellular Signaling Peptides and Proteins - genetics | Monosaccharide Transport Proteins - metabolism | Peptide Fragments - genetics | Protein-Serine-Threonine Kinases - metabolism | Monosaccharide Transport Proteins - genetics | Membrane Proteins - genetics | Phagosomes - metabolism | Recombinant Proteins - chemistry | Antiporters - metabolism | Recombinant Fusion Proteins - chemistry | Huntingtin Protein | Peptide Fragments - chemistry | Models, Biological | Protein-Serine-Threonine Kinases - chemistry | Antiporters - antagonists & inhibitors | Hepatocytes - enzymology | Autophagy-Related Proteins | Phagosomes - enzymology | Cricetulus | Hepatocytes - metabolism | Autophagy | Recombinant Fusion Proteins - metabolism | Autophagy-Related Protein-1 Homolog | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Hepatocytes - cytology | Nerve Tissue Proteins - chemistry | Antiporters - genetics | Membrane Proteins - metabolism | Protein Interaction Domains and Motifs | Monosaccharide Transport Proteins - antagonists & inhibitors | Recombinant Proteins - metabolism | Cell Line | Peptide Fragments - metabolism | Vesicular Transport Proteins - genetics | Protein-Serine-Threonine Kinases - genetics | Mutant Proteins - metabolism | Vesicular Transport Proteins - chemistry | Recombinant Proteins - genetics | Nerve Tissue Proteins - genetics | Protein Transport | Nerve Tissue Proteins - metabolism | Animals | Membrane Proteins - chemistry | Intracellular Signaling Peptides and Proteins - chemistry | Mutant Proteins - chemistry | Amino Acid Substitution | Phosphates | Enzymes | Glucose | Analysis | Dextrose
Journal Article
The EMBO Journal, ISSN 0261-4189, 01/2018, Volume 37, Issue 2, pp. 282 - 299
... and in vivo assays, we have identified a trimeric chaperone complex (Hsc70, Hsp110, and J‐protein) that completely suppresses fibrilization of HttExon1Q48... 
suppression | disaggregation | molecular chaperones | HttpolyQ | NPCs | EXPANDED HUNTINGTIN | HSP70 | PROTEIN AGGREGATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DRUG DISCOVERY | TOXICITY | CELLULAR-MODEL | CELL BIOLOGY | DISEASE | POLYGLUTAMINE AGGREGATION | STRESS | ATP | Neurons - pathology | HSC70 Heat-Shock Proteins - metabolism | Humans | Huntington Disease - pathology | Multiprotein Complexes - genetics | HSP110 Heat-Shock Proteins - chemistry | Multiprotein Complexes - metabolism | Protein Aggregation, Pathological - pathology | HEK293 Cells | Neurons - metabolism | HSP40 Heat-Shock Proteins - chemistry | Protein Aggregation, Pathological - genetics | HSC70 Heat-Shock Proteins - genetics | HSP40 Heat-Shock Proteins - metabolism | HSP40 Heat-Shock Proteins - genetics | Huntingtin Protein - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Caenorhabditis elegans | HSP110 Heat-Shock Proteins - genetics | Multiprotein Complexes - chemistry | Animals | HSC70 Heat-Shock Proteins - chemistry | Huntington Disease - genetics | Huntingtin Protein - genetics | HSP110 Heat-Shock Proteins - metabolism | Protein Aggregation, Pathological - metabolism | Huntingtons disease | Polyglutamine | Huntingtin | Neurodegenerative diseases | Fibrils | Trinucleotide repeats | Disaggregation | Agglomeration | Chaperones | Huntington's disease | Mammalian cells | Proteins | Fibrillogenesis | Hsc70 protein | Neuroscience | Protein Biosynthesis & Quality Control | Molecular Biology of Disease
Journal Article
PLoS genetics, ISSN 1553-7404, 2018, Volume 14, Issue 4, p. e1007363
.... Mutations in subunits of the heterotetrameric (ε-β4-μ4-σ4) adaptor protein 4 (AP-4) complex cause an autosomal recessive form of complicated HSP re 
INTELLECTUAL DISABILITY | RECESSIVE LOSS | COMPLEX-4 AP-4 | HEREDITARY SPASTIC PARAPLEGIA | ALZHEIMERS-DISEASE | CORPUS-CALLOSUM | ADAPTER | GENETICS & HEREDITY | VICI SYNDROME | AMYLOID PRECURSOR PROTEIN | AUTOPHAGY | Receptors, Glutamate - metabolism | Spastic Paraplegia, Hereditary - genetics | Spinal Cord - metabolism | Vesicular Transport Proteins - metabolism | Humans | Adaptor Protein Complex 4 - chemistry | Male | Adaptor Protein Complex 4 - genetics | Spastic Paraplegia, Hereditary - metabolism | Brain - metabolism | trans-Golgi Network - metabolism | Protein Aggregates - genetics | Spinal Cord - pathology | Adaptor Protein Complex 4 - deficiency | Female | Membrane Proteins - metabolism | Neurons - metabolism | Spastic Paraplegia, Hereditary - pathology | Protein Aggregation, Pathological - genetics | Disease Models, Animal | Adaptor Protein Complex Subunits - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Axons - metabolism | Behavior, Animal - physiology | Adaptor Protein Complex Subunits - chemistry | Huntingtin Protein - chemistry | Mice, Knockout | Animals | Brain - pathology | Mice | Huntingtin Protein - genetics | Mutation | Autophagy-Related Proteins - metabolism | Adaptor Protein Complex Subunits - genetics | Protein Aggregation, Pathological - metabolism | Development and progression | Genetic aspects | Diagnosis | Paralysis, Spastic | Spinal cord | Neurosciences | Huntingtin | Funding | Intellectual disabilities | Genes | Neurobiology | Childrens health | Biology | Microcephaly | Autophagy | Proteins | Fibroblasts | Paralysis | Seizures | Phenotypes | Language disorders | Neurons | Spasticity | Corpus callosum | Golgi apparatus | Axons | Microencephaly | Skin | Dystrophy | Phagocytosis | Cytoplasm
Journal Article
The FEBS journal, ISSN 1742-4658, 2017, Volume 284, Issue 9, pp. 1279 - 1295
Journal Article
EMBO reports, ISSN 1469-3178, 2009, Volume 10, Issue 2, pp. 173 - 179
Ubiquilins (UBQLNs) are adaptor proteins thought to deliver ubiquitinated substrates to proteasomes... 
ubiquitin‐like | PLIC | autophagy | ubiquilin | autophagosomes | APOPTOSIS | ubiquitin-like | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL AUTOPHAGY | MITOPHAGY | DEATH | MATURATION | HUNTINGTIN | INCLUSION-BODY FORMATION | CELL BIOLOGY | PROTEASOME | DEGRADATION | PROMOTES | Ubiquitin-Activating Enzymes - physiology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Ubiquitins - genetics | Humans | Adaptor Proteins, Vesicular Transport - genetics | Recombinant Fusion Proteins - physiology | Autophagy - physiology | Autophagy - drug effects | Microscopy, Immunoelectron | Cell Cycle Proteins - antagonists & inhibitors | Recombinant Fusion Proteins - antagonists & inhibitors | RNA Interference | Cell Cycle Proteins - genetics | Carrier Proteins - physiology | Protein Structure, Tertiary | Ubiquitin-Activating Enzymes - genetics | Adaptor Proteins, Vesicular Transport - physiology | Adaptor Proteins, Vesicular Transport - antagonists & inhibitors | Phagosomes - metabolism | Carrier Proteins - antagonists & inhibitors | RNA, Small Interfering - physiology | Microtubule-Associated Proteins - antagonists & inhibitors | Ubiquitins - physiology | HeLa Cells - drug effects | Microtubule-Associated Proteins - physiology | Protein Interaction Mapping | Carrier Proteins - genetics | Autophagy-Related Protein 7 | Animals | Autophagy-Related Protein 5 | Ubiquitin-Activating Enzymes - antagonists & inhibitors | Culture Media - pharmacology | Mice | HeLa Cells - cytology | Cell Cycle Proteins - physiology | Ubiquitins - antagonists & inhibitors | Proteins | Genetics | Nutrients | Molecular biology | Substrates | Scientific Report
Journal Article
Nature Communications, ISSN 2041-1723, 04/2015, Volume 6, Issue 1, p. 6768
The brain has a limited capacity to self-protect against protein aggregate-associated pathology, and mounting evidence supports a role for phagocytic glia in this process... 
MOTOR-NEURONS | CELLS | IN-VITRO | ACTIVATION | ENGULFMENT | MULTIDISCIPLINARY SCIENCES | MUTANT HUNTINGTIN | DISEASE | TAU | PATHOLOGY | PROPAGATION | Protein Aggregates | Neurons - pathology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Neuroglia - pathology | Humans | Huntington Disease - pathology | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Brain - metabolism | Drosophila melanogaster - metabolism | Molecular Mimicry | Membrane Proteins - metabolism | Neurons - metabolism | Protein Aggregation, Pathological - genetics | Genes, Reporter | Disease Models, Animal | Neuroglia - chemistry | Prions - metabolism | Neurons - chemistry | Signal Transduction | Membrane Proteins - genetics | Bacterial Proteins - genetics | Gene Expression Regulation | Prions - chemistry | Huntington Disease - metabolism | Disease Progression | Huntingtin Protein | Animals | Brain - pathology | Huntington Disease - genetics | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Neuroglia - metabolism | Drosophila Proteins - genetics | Mutation | Phagocytosis | Protein Aggregation, Pathological - metabolism | Luminescent Proteins - metabolism | Draper protein | Neuroprotection | Brain | Huntingtin | Neurodegenerative diseases | Pathogenesis | Drosophila | Conversion | Neuronal-glial interactions | Proteins | Neurological diseases | Phagocytes | Signal transduction | Aggregates | Insects | Cytoplasm
Journal Article