IndraLab

Statements

reach
"We demonstrate that discrete functions of ADAR1p150 determine MDA5 or PKR engagement: A-to-I editing of endogenous dsRNA specifically prevents MDA5 activation, whereas PKR activation is prevented by e[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"ADAR1-mediated dsRNA editing prevents the activation of MDA5, the endogenous sensing system of cytoplasmic dsRNA, thereby inhibiting cell apoptosis [ 3 ]."
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"ADAR1-edited dsRNA inhibits MDA5 and Rig1 activation (Figure 1a) [41]⁠."
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"For immunology, dsRNA containing multiple groups of I/U inhibits the activity of MDA5, RIG1 and IRF-3, thus inhibiting the induction pathway of IFN-I and affecting the host antiviral response (5, 28) (Figure 4)."
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"Editing of dsRNA through co-transcriptional ADAR-mediated A-I editing prevents downstream Type-I-Interferon activation of MDA5 (Figure 1B) by creating wobble A-I base pairs so that MDA5 cannot recognize endogenous dsRNA [51,54,70]."
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"Taken together, the results indicated that certain sites in the 3’UTR are efficiently edited by a very limited amount of ADAR1 p150 in the mouse brain, which might affect the dsRNA structure required to prevent MDA5 activation."
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"Immunofluorescence analysis using specific dsRNA antibodies showed a significant and time-dependent accumulation of dsRNA in the USP18 KO cells after IFN treatment, indicating that USP18-dependent ISGylation under these conditions could inhibit ADAR activity.In addition to ADAR, PKR, RIG-I and MDA5, we found other proteins involved in antigen presentation and resistance to immunotherapy, such as TAP1, GBP1, STAT1, IFIT1, PSMB10, PSMB9, GBP2, MAGE and PARP14, also regulated by USP18-dependent ISGylation."
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"PKR is an intracellular protein that binds dsRNA in a length-dependent fashion and induces apoptosis in the host cell to prevent viral propagation.12 TLR3 , MDA5 , and RIG-I also recognize dsRNA and play an active role in immune activation ."
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"Mechanistically, adenosine-to-inosine (A-to-I) base modification of endogenous dsRNA by ADAR1 prevents chronic overactivation of the dsRNA sensors MDA5 and PKR 3,7-10,13,14 ."
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"A-to-I deamination of dsRNA by adenosine deaminase RNA-specific (ADAR1), which weakens base pairing and causes bulges, is nevertheless required to prevent MDA5-dependent autoinflammatory signaling induced by endogenous RNAs with high double-stranded content, for example, annealed inverted Alu repeats (27, 28, 29, 30)."
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"Another possibility is that inosine in dsRNA prevents the activation of MDA5, locking it in an off position so that only a few inosine containing transcripts are required."
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"A-to-I editing by ADAR1 creates bulges in the dsRNA structure that prevent MDA5 recognition, allowing cancer cells with upregulated ADAR1 to circumvent viral mimicry activation."
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