期刊
SCIENTIFIC REPORTS
卷 2, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep01016
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资金
- UK Medical Research Council
- Motor Neurone Disease Association
- Alzheimer's Research UK
- MHMS General Charitable Trust
- Medical Research Council/Motor Neurone Disease Association Lady Edith Wolfson Fellowship
- Alzheimers Research UK [ARUK-PPG2012A-14] Funding Source: researchfish
- Medical Research Council [G1000287, G0500288] Funding Source: researchfish
- MRC [G0500288, G1000287] Funding Source: UKRI
Large expansions of a non-coding GGGGCC-repeat in the first intron of the C9orf72 gene are a common cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). G-rich sequences have a propensity for forming highly stable quadruplex structures in both RNA and DNA termed G-quadruplexes. G-quadruplexes have been shown to be involved in a range of processes including telomere stability and RNA transcription, splicing, translation and transport. Here we show using NMR and CD spectroscopy that the C9orf72 hexanucleotide expansion can form a stable G-quadruplex, which has profound implications for disease mechanism in ALS and FTD.
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