Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase

By M. Faghihi, Farzaneh Modarresi, A. Khalil, Douglas E. Wood, B. Sahagan, T. Morgan, C. Finch, G. Laurent, P. Kenny, Claes Wahlestedt. Nature Medicine, 2008

1,388 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Plant Science

View Paper: https://www.semanticscholar.org/paper/edb836760eccbe4a8e715d08d5d50e2ac18400cd

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Citations in the corpus

LincRNA-p21 suppresses target mRNA translation. (2012, background): “LncRNAs have also been reported to participate in a limited number of posttranscriptional processes: the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was implicated in splicing, the cytoplasmic half-Staufen 1-binding site lncRNAs (1/2-sbsRNAs) was implicated in Staufen 1-me”
Non‐coding RNAs: regulators of disease (2010, background): “It is not surprising, then, that the dysregulation of lncRNAs appears to be a primary feature of many complex human diseases, including leukaemia [175], colon cancer [176], prostate cancer [177], breast cancer [178], hepatocellular carcinoma [175,179], psoriasis [180], ischaemic heart disease [181,1”
Evolution and functions of long noncoding RNAs. (2009, background): “For example, increased expression of either BC200 or an antisense transcript of the b-secretase-1 (BACE1) gene has been implicated in the progression of Alzheimer’s disease (Faghihi et al., 2008; Mus et al., 2007).”
Inhibiting DNA methylation causes an interferon response in cancer via dsRNA including endogenous retroviruses (2015, neutral): “Such sense and antisense transcripts can form dsRNA (Faghihi et al., 2008; Su et al., 2012).”
Long non-coding RNAs and complex diseases: from experimental results to computational models (2016, background): “[102], lung cancer [25, 103], ovarian cancer [104], AD [26], dia-”
Long Noncoding RNAs: Past, Present, and Future (2013, background): “For example, the antisense transcript of the Alzheimer-associated b-secretase-1 (BACE), known as BACEAS, increases BACE mRNA stability (Faghihi et al. 2008), most likely by masking the binding sites for miR-485-5p (Faghihi et al. 2010).”
Long noncoding RNAs: functional surprises from the RNA world. (2009, background): “Recent work on Alzheimer’s disease has identified a ncRNA antisense to the b-secretase (BACE1) gene, which generates amyloid b (Ab), that may aid in driving the disease (Faghihi et al. 2008).”