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Amino acids, ISSN 0939-4451, 3/2017, Volume 49, Issue 3, pp. 501 - 515
Post-translational modification (PTM) is an important mechanism in modulating a protein’s structure and can lead to substantial diversity in biological function... 
Biochemistry, general | Serotonylation | Post-translational modification | Aminylation | Polyaminylation | Neurobiology | Life Sciences | Analytical Chemistry | Life Sciences, general | Biochemical Engineering | Proteomics | Tissue transglutaminase | Histaminylation | TG2 | Life Sciences & Biomedicine | Biochemistry & Molecular Biology | Science & Technology | Cytoskeletal Proteins - genetics | Humans | Substrate Specificity | Transglutaminases - genetics | NF-KappaB Inhibitor alpha - genetics | GTP-Binding Proteins - genetics | Amination | Biogenic Amines - metabolism | Protein Domains | Cytoskeletal Proteins - metabolism | Protein Aggregation, Pathological - genetics | Extracellular Matrix Proteins - metabolism | Signal Transduction | Extracellular Matrix Proteins - genetics | Huntingtin Protein - metabolism | Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - genetics | Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism | Animals | Histones - genetics | NF-KappaB Inhibitor alpha - metabolism | Transglutaminases - metabolism | Protein Processing, Post-Translational | Histones - metabolism | Huntingtin Protein - genetics | Biogenic Amines - chemistry | Protein Aggregation, Pathological - metabolism | GTP-Binding Proteins - metabolism | Proteins | Physiological aspects | Medical colleges | Community colleges | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 04/2017, Volume 545, Issue 7652, pp. 108 - 111
Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and ataxin 3 in spinocerebellar ataxia type 3 (SCA3)(1,2... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Humans | Ubiquitin - metabolism | Male | Neurons - cytology | Autophagy | Brain - metabolism | Peptides - metabolism | Protein Domains | Ataxin-3 - chemistry | Female | Food Deprivation | Neurons - metabolism | Protein Stability | Ataxin-3 - metabolism | Disease Models, Animal | Binding, Competitive | Cell Line | Ataxin-3 - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Cells, Cultured | Mutant Proteins - genetics | Exons - genetics | Mutant Proteins - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Animals | Mutant Proteins - chemistry | Brain - pathology | Huntington Disease - genetics | Protein Binding | Mice | Huntingtin Protein - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | Beclin-1 - metabolism | Ataxin-3 - genetics | Physiological aspects | Autophagy (Cytology) | Neural circuitry | Observations | Huntingtons disease | Competition | Biotechnology | Huntingtin | Toxicity | Pathogenesis | Impairment | Biosynthesis | Kinases | Experiments | Degradation | Proteins | Scholarships & fellowships | Ataxin | Rodents | Spinocerebellar ataxia | Ataxia | Biocompatibility | Trinucleotide repeat diseases | Medical research | Starvation | Neurodegenerative diseases | Polyglutamine diseases | Huntington's disease | Neurological diseases | Machado-Joseph disease | Cell lines | Scientific imaging | Mass spectrometry | Phagocytosis | Index Medicus
Journal Article
Journal Article