Poly(GP) proteins are a useful pharmacodynamic marker for C9ORF72 -associated amyotrophic lateral sclerosis
Published 2017 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Poly(GP) proteins are a useful pharmacodynamic marker for
C9ORF72
-associated amyotrophic lateral sclerosis
Authors
Keywords
-
Journal
Science Translational Medicine
Volume 9, Issue 383, Pages eaai7866
Publisher
American Association for the Advancement of Science (AAAS)
Online
2017-03-30
DOI
10.1126/scitranslmed.aai7866
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Timing and significance of pathological features inC9orf72expansion-associated frontotemporal dementia
- (2016) Sarat C. Vatsavayai et al. BRAIN
- There has been an awakening: Emerging mechanisms of C9orf72 mutations in FTD/ALS
- (2016) Aaron D. Gitler et al. BRAIN RESEARCH
- Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs
- (2016) Jie Jiang et al. NEURON
- Spt4 selectively regulates the expression of C9orf72 sense and antisense mutant transcripts
- (2016) N. J. Kramer et al. SCIENCE
- Cerebellar c9RAN proteins associate with clinical and neuropathological characteristics of C9ORF72 repeat expansion carriers
- (2015) Tania F. Gendron et al. ACTA NEUROPATHOLOGICA
- Novel clinical associations with specific C9ORF72 transcripts in patients with repeat expansions in C9ORF72
- (2015) Marka van Blitterswijk et al. ACTA NEUROPATHOLOGICA
- Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing
- (2015) Martin H. Schludi et al. ACTA NEUROPATHOLOGICA
- Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis
- (2015) Jonathan D Rohrer et al. LANCET NEUROLOGY
- The C9orf72 repeat expansion disrupts nucleocytoplasmic transport
- (2015) Ke Zhang et al. NATURE
- Brain morphologic changes in asymptomaticC9orf72repeat expansion carriers
- (2015) Renée Walhout et al. NEUROLOGY
- C9orf72 BAC Transgenic Mice Display Typical Pathologic Features of ALS/FTD
- (2015) Jacqueline G. O’Rourke et al. NEURON
- C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits
- (2015) J. Chew et al. SCIENCE
- Mechanisms of toxicity in C9FTLD/ALS
- (2014) Tania F. Gendron et al. ACTA NEUROPATHOLOGICA
- Discovery of a Biomarker and Lead Small Molecules to Target r(GGGGCC)-Associated Defects in c9FTD/ALS
- (2014) Zhaoming Su et al. NEURON
- Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins
- (2013) Kohji Mori et al. ACTA NEUROPATHOLOGICA
- Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS
- (2013) Tania F. Gendron et al. ACTA NEUROPATHOLOGICA
- Pathophysiological insights into ALS with C9ORF72 expansions
- (2013) K. L. Williams et al. JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
- An antisense oligonucleotide against SOD1 delivered intrathecally for patients with SOD1 familial amyotrophic lateral sclerosis: a phase 1, randomised, first-in-man study
- (2013) Timothy M Miller et al. LANCET NEUROLOGY
- Association between repeat sizes and clinical and pathological characteristics in carriers of C9ORF72 repeat expansions (Xpansize-72): a cross-sectional cohort study
- (2013) Marka van Blitterswijk et al. LANCET NEUROLOGY
- Unconventional Translation of C9ORF72 GGGGCC Expansion Generates Insoluble Polypeptides Specific to c9FTD/ALS
- (2013) Peter E.A. Ash et al. NEURON
- RNA Toxicity from the ALS/FTD C9ORF72 Expansion Is Mitigated by Antisense Intervention
- (2013) Christopher J. Donnelly et al. NEURON
- RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia
- (2013) T. Zu et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration
- (2013) C. Lagier-Tourenne et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS
- (2013) K. Mori et al. SCIENCE
- Targeting RNA Foci in iPSC-Derived Motor Neurons from ALS Patients with a C9ORF72 Repeat Expansion
- (2013) D. Sareen et al. Science Translational Medicine
- Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS
- (2011) Mariely DeJesus-Hernandez et al. NEURON
- A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD
- (2011) Alan E. Renton et al. NEURON
- Consensus criteria for the diagnosis of frontotemporal cognitive and behavioural syndromes in amyotrophic lateral sclerosis
- (2009) Michael J. Strong et al. Amyotrophic Lateral Sclerosis
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExploreDiscover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversation