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1. Full Text SRSF1-dependent nuclear export inhibition of C9ORF72 repeat transcripts prevents neurodegeneration and associated motor deficits
by Hautbergue, Guillaume M and Castelli, Lydia M and Ferraiuolo, Laura and Sanchez-Martinez, Alvaro and Cooper-Knock, Johnathan and Higginbottom, Adrian and Lin, Ya-Hui and Bauer, Claudia S and Dodd, Jennifer E and Myszczynska, Monika A and Alam, Sarah M and Garneret, Pierre and Chandran, Jayanth S and Karyka, Evangelia and Stopford, Matthew J and Smith, Emma F and Kirby, Janine and Meyer, Kathrin and Kaspar, Brian K and Isaacs, Adrian M and El-Khamisy, Sherif F and De Vos, Kurt J and Ning, Ke and Azzouz, Mimoun and Whitworth, Alexander J and Shaw, Pamela J
Nature Communications, ISSN 2041-1723, 07/2017, Volume 8, Issue 1, pp. 16063 - 16063
Hexanucleotide repeat expansions in the C9ORF72 gene are the commonest known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia.... 
SPINAL MUSCULAR-ATROPHY | DROSOPHILA MODEL | MULTIDISCIPLINARY SCIENCES | FRONTOTEMPORAL DEMENTIA | BINDING PROTEINS | GENE-EXPRESSION | MESSENGER-RNA EXPORT | HEXANUCLEOTIDE REPEAT | GGGGCC REPEAT | SPORADIC ALS | NUCLEOCYTOPLASMIC TRANSPORT | Cell Line | Coculture Techniques | Drosophila | Humans | Middle Aged | Rats | Male | Nuclear Proteins - metabolism | Serine-Arginine Splicing Factors - metabolism | Frontotemporal Dementia - metabolism | Transcription Factors - metabolism | Astrocytes - physiology | Animals | Nucleocytoplasmic Transport Proteins - metabolism | Frontotemporal Dementia - etiology | Amyotrophic Lateral Sclerosis - metabolism | Adult | Female | Aged | C9orf72 Protein - metabolism | Mice | Amyotrophic Lateral Sclerosis - etiology | RNA-Binding Proteins - metabolism | Disease Models, Animal | Intervention | Neuroprotection | Cell culture | Animal models | Neurons | Amyotrophic lateral sclerosis | Motor task performance | Assaying | Nuclear transport | Exports | Proteins | Neurotoxicity | Depletion | Ribonucleic acids | Insects | Neurodegeneration | Cell death | Dementia disorders | Inhibition | Frontotemporal dementia | Index Medicus
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2. Full Text The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy
by Webster, Christopher P and Smith, Emma F and Bauer, Claudia S and Moller, Annekathrin and Hautbergue, Guillaume M and Ferraiuolo, Laura and Myszczynska, Monika A and Higginbottom, Adrian and Walsh, Matthew J and Whitworth, Alexander J and Kaspar, Brian K and Meyer, Kathrin and Shaw, Pamela J and Grierson, Andrew J and De Vos, Kurt J
The EMBO Journal, ISSN 0261-4189, 08/2016, Volume 35, Issue 15, pp. 1656 - 1676
A GGGGCC hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia... 
Rab GTPase | frontotemporal dementia | autophagy | amyotrophic lateral sclerosis | C9orf72 | MOTOR-NEURONS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALS | NEURODEGENERATION | AMYOTROPHIC-LATERAL-SCLEROSIS | FRONTOTEMPORAL LOBAR DEGENERATION | CELL BIOLOGY | ANTISENSE TRANSCRIPTS | EXPANSION | ABLATION | HEXANUCLEOTIDE REPEAT | RNA FOCI | Proteins - metabolism | Neurons - chemistry | rab1 GTP-Binding Proteins - metabolism | Humans | Cell Physiological Phenomena | Cells, Cultured | Autophagy-Related Protein-1 Homolog - metabolism | C9orf72 Protein | Intracellular Signaling Peptides and Proteins - metabolism | Neurons - metabolism | Autophagy | Frontotemporal Dementia - pathology | Amyotrophic lateral sclerosis | Frontotemporal dementia | Proteins | Pathology | Genetics | Neuroscience
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3. Full Text Antisense RNA foci in the motor neurons of C9ORF72-ALS patients are associated with TDP-43 proteinopathy
by Cooper-Knock, Johnathan and Higginbottom, Adrian and Stopford, Matthew J and Highley, J Robin and Ince, Paul G and Wharton, Stephen B and Pickering-Brown, Stuart and Kirby, Janine and Hautbergue, Guillaume M and Shaw, Pamela J
Acta Neuropathologica, ISSN 0001-6322, 7/2015, Volume 130, Issue 1, pp. 63 - 75
GGGGCC repeat expansions of C9ORF72 represent the most common genetic variant of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We and others... 
Immunohistochemistry | Pathology | Neurosciences | Dipeptide repeat protein | Medicine & Public Health | Amyotrophic lateral sclerosis | C9ORF72 | RNA foci | EXPANSIONS | ALS | NEURODEGENERATION | AMYOTROPHIC-LATERAL-SCLEROSIS | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | TRANSLATION | NEUROSCIENCES | CLINICAL NEUROLOGY | SEQUESTRATION | MESSENGER-RNA | DIPEPTIDE-REPEAT PROTEINS | HEXANUCLEOTIDE REPEAT | Frontotemporal Lobar Degeneration - pathology | Humans | Middle Aged | Male | Motor Neurons - pathology | DNA-Binding Proteins - metabolism | DNA Repeat Expansion | Frontotemporal Lobar Degeneration - metabolism | Female | C9orf72 Protein | Inclusion Bodies - metabolism | RNA, Antisense | Purkinje Cells - metabolism | Amyotrophic Lateral Sclerosis - genetics | Cerebellum - metabolism | Hippocampus - pathology | Cerebellum - pathology | Motor Neurons - metabolism | Proteins - genetics | Hippocampus - metabolism | Amyotrophic Lateral Sclerosis - pathology | Inclusion Bodies - genetics | Proteins - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Inclusion Bodies - pathology | Frontotemporal Lobar Degeneration - genetics | Purkinje Cells - pathology | Proteins | Crosslinked polymers | Neurons | Antisense RNA | Protein binding | Index Medicus | Original Paper
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4. Full Text C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis
by Cooper-Knock, Johnathan and Bury, Joanna J and Heath, Paul R and Wyles, Matthew and Higginbottom, Adrian and Gelsthorpe, Catherine and Highley, J. Robin and Hautbergue, Guillaume and Rattray, Magnus and Kirby, Janine and Shaw, Pamela J
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, p. e0127376
Objective An intronic GGGGCC-repeat expansion of C9ORF72 is the most common genetic variant of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.... 
MULTIDISCIPLINARY SCIENCES | EXPANSION | FTD | MUTATIONS | PROTEINS | SENSE | HEXANUCLEOTIDE REPEAT | FAMILIAL ALS | ONSET | RNA FOCI | DEGENERATION | Cell Line | Reproducibility of Results | DNA Repeat Expansion - genetics | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Male | Gene Expression Profiling | Motor Neurons - metabolism | Amyotrophic Lateral Sclerosis - pathology | RNA Splicing - genetics | Adult | Female | Aged | Gene Ontology | Care and treatment | Patient outcomes | Amyotrophic lateral sclerosis | Development and progression | Antisense RNA | Research | Risk factors | Protein binding | Dementia | Biotechnology | Neurosciences | Genes | Gene regulation | Consistency | Proteins | Neurodegeneration | Dementia disorders | RNA processing | Bioinformatics | Expansion | Deoxyribonucleic acid--DNA | Binding | Motor neurons | Cell survival | Splicing | Nucleotide sequence | Neurons | Lymphoblastoid cell lines | Gene expression | Ribonucleic acid--RNA | Patients | Genetic variance | Correlation analysis | Frontotemporal dementia | Alzheimers disease | RNA | Deoxyribonucleic acid | Ribonucleic acid | DNA
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5. Full Text C9orf72 expansion disrupts ATM-mediated chromosomal break repair
by Walker, Callum and Herranz-Martin, Saul and Karyka, Evangelia and Liao, Chunyan and Lewis, Katherine and Elsayed, Waheba and Lukashchuk, Vera and Chiang, Shih-Chieh and Ray, Swagat and Mulcahy, Padraig J and Jurga, Mateusz and Tsagakis, Ioannis and Iannitti, Tommaso and Chandran, Jayanth and Coldicott, Ian and De Vos, Kurt J and Hassan, Mohamed K and Higginbottom, Adrian and Shaw, Pamela J and Hautbergue, Guillaume M and Azzouz, Mimoun and El-Khamisy, Sherif F
Nature Neuroscience, ISSN 1097-6256, 09/2017, Volume 20, Issue 9, pp. 1225 - 1235
Hexanucleotide repeat expansions represent the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the... 
DNA | UBIQUITIN | 53BP1 | TRANSCRIPTION | DISEASE | DIPEPTIDE REPEAT PROTEINS | ATAXIA | ACCUMULATION | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | R LOOPS | DNA Repeat Expansion - physiology | Spinal Cord - metabolism | Ataxia Telangiectasia Mutated Proteins - metabolism | Amyotrophic Lateral Sclerosis - genetics | Humans | Mice, Inbred C57BL | Cells, Cultured | DNA Repair - physiology | Rats | Random Allocation | Proteins - genetics | Amyotrophic Lateral Sclerosis - pathology | Animals | Proteins - metabolism | Spinal Cord - pathology | Amyotrophic Lateral Sclerosis - metabolism | HEK293 Cells | C9orf72 Protein | Mice | Ataxia Telangiectasia Mutated Proteins - genetics | Chromosome Breakage | Chromosome abnormalities | Gene mutations | Nervous system | Development and progression | Degeneration | Genetic aspects | Open reading frames | Health aspects | Ubiquitin | Spinal cord | Hybrids | Stability | DNA damage | Central nervous system | Amyotrophic lateral sclerosis | Viruses | Gene expression | Tissues | Ribonucleic acid--RNA | DNA repair | Accumulation | Genomic instability | Neurodegeneration | Bioaccumulation | Dementia disorders | R-loops | Frontotemporal dementia | Repair | Damage accumulation | Deoxyribonucleic acid--DNA
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6. Full Text Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS)
by Cox, Laura E and Ferraiuolo, Laura and Goodall, Emily F and Heath, Paul R and Higginbottom, Adrian and Mortiboys, Heather and Hollinger, Hannah C and Hartley, Judith A and Brockington, Alice and Burness, Christine E and Morrison, Karen E and Wharton, Stephen B and Grierson, Andrew J and Ince, Paul G and Kirby, Janine and Shaw, Pamela J
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 3, p. e9872
Background: Amyotrophic lateral sclerosis (ALS), a common late-onset neurodegenerative disease, is associated with fronto-temporal dementia (FTD) in 3-10% of... 
CELLULAR PATHWAYS | COMPLEX | PROTEIN | ESCRT-III | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | AUTOPHAGY | FRONTOTEMPORAL LOBAR DEGENERATION | MUSCULAR-ATROPHY | COMMON-CAUSE | Oligonucleotide Array Sequence Analysis | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Cercopithecus aethiops | Endosomal Sorting Complexes Required for Transport - genetics | England | Male | Neurodegenerative Diseases - therapy | Mutation, Missense | Nerve Tissue Proteins - genetics | Motor Neurons - metabolism | Animals | DNA Mutational Analysis | Spinal Cord - pathology | Brain - pathology | Female | Aged | Mutation | COS Cells | Nervous system diseases | DNA microarrays | Neurons | Analysis | Genetic research | Amyotrophic lateral sclerosis | Genetic aspects | Gene expression | Huntingtons disease | Neurosciences | Calcium | Pathogenesis | Cytology | Nervous system | Cases (containers) | Kinases | Autophagy | Defects | Proteins | Atrophy | Signal transduction | Carcinogens | Missense mutation | Transfection | Neurodegeneration | Dementia disorders | Genetics | Stress response | Motor neurons | Pathogens | CD63 antigen | MAP kinase | Patients | Pathogenicity | Signaling | Pedigree | Aberration | Frontotemporal dementia | Dismantling | Vacuoles | Phagocytosis | Apoptosis | Dementia
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7. Full Text CD81 Is Required for Hepatitis C Virus Glycoprotein-Mediated Viral Infection
by Jie Zhang and Glenn Randall and Adrian Higginbottom and Peter Monk and Charles M. Rice and Jane A. McKeating
Journal of Virology, ISSN 0022-538X, 02/2004, Volume 78, Issue 3, pp. 1448 - 1455
Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
HEMATOPOIETIC-CELLS | IN-VITRO | VIROLOGY | DC-SIGN | PROTEIN COMPLEXES | STRAND RNA | CELL-LINES | ENVELOPE PROTEINS | HIV-1 INFECTION | BINDING | DENSITY-LIPOPROTEIN RECEPTOR | Cell Line | Viral Envelope Proteins - genetics | Membrane Glycoproteins - metabolism | Receptors, Virus - metabolism | Humans | Hepacivirus - genetics | Hepacivirus - pathogenicity | Tetraspanin 28 | HIV-1 - genetics | Antigens, CD - metabolism | Membrane Glycoproteins - genetics | Viral Structural Proteins - genetics | Animals | HIV-1 - physiology | Lymphocytes - virology | Epithelial Cells - virology | Viral Envelope Proteins - metabolism | HIV Envelope Protein gp160 - genetics | Hepatocytes - virology | Hepacivirus - physiology | Membrane Proteins - metabolism | Mice | Viral Structural Proteins - metabolism | HIV Envelope Protein gp160 - metabolism | Virus-Cell Interactions
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8. Full Text Viral Delivery of Antioxidant Genes as a Therapeutic Strategy in Experimental Models of Amyotrophic Lateral Sclerosis
by Nanou, Aikaterini and Higginbottom, Adrian and Valori, Chiara F and Wyles, Matthew and Ning, Ke and Shaw, Pamela and Azzouz, Mimoun
Molecular Therapy, ISSN 1525-0016, 08/2013, Volume 21, Issue 8, pp. 1486 - 1496
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder with no effective treatment to date. Despite its multi-factorial aetiology,... 
MEDICINE, RESEARCH & EXPERIMENTAL | MOTOR-NEURON INJURY | OXIDATIVE DAMAGE | SPINAL-CORD | FAMILIAL ALS | OLIGONUCLEOTIDE MICROARRAY | PEROXIREDOXIN SUBTYPES | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | DISEASE | GENETICS & HEREDITY | MUTANT SOD1 | MICE | HEXANUCLEOTIDE REPEAT | Cell Line | Dependovirus - genetics | Gene Transfer Techniques | Genetic Therapy | Gene Expression | Superoxide Dismutase - genetics | Transduction, Genetic | Signal Transduction | Amyotrophic Lateral Sclerosis - therapy | Amyotrophic Lateral Sclerosis - genetics | Humans | Oxidative Stress - genetics | Mice, Transgenic | Genetic Vectors - genetics | Motor Neurons - metabolism | Peroxiredoxin III - genetics | Animals | Lentivirus - genetics | NF-E2-Related Factor 2 - genetics | Mice | Transgenes | Superoxide Dismutase - metabolism | Astrocytes - metabolism | Disease Models, Animal | Original
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9. Full Text TDP-43 induces p53-mediated cell death of cortical progenitors and immature neurons
by Vogt, Miriam A and Ehsaei, Zahra and Knuckles, Philip and Higginbottom, Adrian and Helmbrecht, Michaela S and Kunath, Tilo and Eggan, Kevin and Williams, Luis A and Shaw, Pamela J and Wurst, Wolfgang and Floss, Thomas and Huber, Andrea B and Taylor, Verdon
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 1 - 13
( TAR DNA-binding protein 43 (TDP-43) is a key player in neurodegenerative diseases including frontotemporal lobar degeneration (FTLD) and amyotrophic lateral... 
PLURIPOTENT STEM-CELLS | PROTEIN | RNA TARGETS | FUS | MULTIDISCIPLINARY SCIENCES | NUCLEAR FACTOR TDP-43 | ALS | BINDING-PROPERTIES | ENDOGENOUS TDP-43 | TRANSGENIC MOUSE MODEL | P53 | Cell proliferation | Bax protein | Neurodegenerative diseases | p53 Protein | Cortex | Amyotrophic lateral sclerosis | Embryos | Progenitor cells | DNA-binding protein | Cell death | Neurodegeneration | Neural stem cells | Frontotemporal dementia | Pluripotency | Apoptosis
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10. Full Text Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions
by Cooper-Knock, Johnathan and Walsh, Matthew J and Higginbottom, Adrian and Highley, J. Robin and Dickman, Mark J and Edbauer, Dieter and Ince, Paul G and Wharton, Stephen B and Wilson, Stuart A and Kirby, Janine and Hautbergue, Guillaume M and Shaw, Pamela J
Brain, ISSN 0006-8950, 2014, Volume 137, Issue 7, pp. 2040 - 2051
GGGGCC repeat expansions of C9orf72 represent the most common genetic variant of amyotrophic lateral sclerosis and frontotemporal degeneration, but the... 
genetics | pathology | amyotrophic lateral sclerosis | fluorescence imaging | AMYOTROPHIC-LATERAL-SCLEROSIS | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | FOCI | CLINICAL NEUROLOGY | MESSENGER-RNA | ANTISENSE TRANSCRIPTS | BINDING PROTEINS | FUNCTIONAL-ANALYSIS | TAP BINDING | HEXANUCLEOTIDE REPEAT | GGGGCC REPEAT | Neurons - pathology | RNA-Binding Proteins - genetics | Phosphorus Isotopes - pharmacokinetics | Biotinylation | DNA Repeat Expansion - genetics | Amyotrophic Lateral Sclerosis - genetics | Humans | Heterogeneous-Nuclear Ribonucleoprotein Group A-B - metabolism | Male | Nuclear Proteins - metabolism | Ribonucleoproteins - metabolism | Heterogeneous Nuclear Ribonucleoprotein A1 | Proteins - genetics | Transcription Factors - metabolism | Amyotrophic Lateral Sclerosis - pathology | Adenosine Triphosphate - pharmacokinetics | Mass Spectrometry | Protein Binding - drug effects | Serine-Arginine Splicing Factors | Brain - pathology | Female | C9orf72 Protein | RNA-Binding Proteins - metabolism | Index Medicus | Abridged Index Medicus | Original
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11. Full Text A neuronal DNA damage response is detected at the earliest stages of Alzheimer's neuropathology and correlates with cognitive impairment in the Medical Research Council's Cognitive Function and Ageing Study ageing brain cohort
by Simpson, Julie E and Ince, Paul G and Matthews, Fiona E and Shaw, Pamela J and Heath, Paul R and Brayne, Carol and Garwood, Claire and Higginbottom, Adrian and Wharton, Stephen B and MRC Cognitive Function Ageing and MRC Cognitive Function and Ageing Neuropathology Study Group
Neuropathology and Applied Neurobiology, ISSN 0305-1846, 06/2015, Volume 41, Issue 4, pp. 483 - 496
Aims Population‐based studies have shown that approximately 20% of the ageing population (aged 65 years and over) with dementia have little or no classical... 
cognitive impairment | DNA‐PKcs | DNA damage response | γH2AX | neurone | DNA-PKcs | Neurone | Cognitive impairment | H2AX | DEMENTIA | INCREASED OXIDATIVE DAMAGE | DEPENDENT PROTEIN-KINASE | NEURODEGENERATION | PATHOLOGY | NEUROSCIENCES | CLINICAL NEUROLOGY | REPAIR | VULNERABLE NEURONS | DISEASE | SENESCENCE | STRESS | RNA OXIDATION | Protein Kinases - metabolism | Pyramidal Cells - metabolism | Oxidative Stress | Humans | Male | Brain - metabolism | Neuropsychological Tests | Alzheimer Disease - metabolism | Aged, 80 and over | Female | Aged | Neurons - metabolism | DNA Damage | Histones - metabolism | Alzheimer Disease - genetics | Alzheimer Disease - psychology | Aging - metabolism | Cohort Studies | Immunohistochemistry | Medical research | Brain | Neurons | DNA damage | Analysis | DNA | Medicine, Experimental | Genetic research | Tumor proteins | DNA repair | Alzheimer's disease | Pathology | Senescence | Brain research | Neuropathology | Cognitive ability | Aging | Deoxyribonucleic acid--DNA | Original
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