Post-translational modifications on RNA-binding proteins: accelerators, brakes, or passengers in neurodegeneration?
- 1 January 2022
- journal article
- review article
- Published by Elsevier in Trends in Biochemical Sciences
- Vol. 47 (1) , 6-22
Abstract
No abstract availableKeywords
This publication has 140 references indexed in Scilit:
- Redox signalling directly regulates TDP‐43 via cysteine oxidation and disulphide cross‐linkingThe EMBO Journal, 2011
- Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementiaNature, 2011
- FET proteins TAF15 and EWS are selective markers that distinguish FTLD with FUS pathology from amyotrophic lateral sclerosis with FUS mutationsBrain, 2011
- Long pre-mRNA depletion and RNA missplicing contribute to neuronal vulnerability from loss of TDP-43Nature Neuroscience, 2011
- ALS‐associated fused in sarcoma (FUS) mutations disrupt Transportin‐mediated nuclear importThe EMBO Journal, 2010
- A new subtype of frontotemporal lobar degeneration with FUS pathologyBrain, 2009
- Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicityProceedings of the National Academy of Sciences, 2009
- Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 ProteinopathiesJournal of Biological Chemistry, 2009
- Phosphorylation of S409/410 of TDP-43 is a consistent feature in all sporadic and familial forms of TDP-43 proteinopathiesActa Neuropathologica, 2009
- Phosphorylated TDP‐43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosisAnnals of Neurology, 2008