| Autor: |
Heraud-Farlow JE; St. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, 3065, Victoria, Australia., Walkley CR; St. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, 3065, Victoria, Australia. cwalkley@svi.edu.au.; Department of Medicine, St. Vincent's Hospital, University of Melbourne, Fitzroy, 3065, Victoria, Australia. cwalkley@svi.edu.au. |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of molecular medicine (Berlin, Germany) [J Mol Med (Berl)] 2016 Oct; Vol. 94 (10), pp. 1095-1102. Date of Electronic Publication: 2016 Apr 05. |
| DOI: |
10.1007/s00109-016-1416-1 |
| Abstrakt: |
The innate immune system is the first line of the cellular defence against invading pathogens. A critical component of this defence is the capacity to discriminate foreign RNA molecules, which are distinct from most cellular RNAs in structure and/or modifications. However, a series of rare autoimmune/autoinflammatory diseases in humans highlight the propensity for the innate immune sensing system to be activated by endogenous cellular double-stranded RNAs (dsRNAs), underscoring the fine line between distinguishing self from non-self. The RNA editing enzyme ADAR1 has recently emerged as a key regulator that prevents innate immune pathway activation, principally the cytosolic dsRNA sensor MDA5, from inducing interferon in response to double-stranded RNA structures within endogenous RNAs. Adenosine-to-Inosine RNA editing by ADAR1 is proposed to destabilise duplexes formed from inverted repetitive elements within RNAs, which appear to prevent MDA5 from sensing these RNA as virus-like in the cytoplasm. Aberrant activation of these pathways has catastrophic effects at both a cellular and organismal level, contributing to one of the causes of the conditions collectively known as the type I interferonopathies. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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