Hirabayashi, R., Hozumi, S., Higashijima, S. Prp5 bridges U1 and U2 snRNPs and enables stable U2 snRNP association with intron RNA. Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq. DEAD-box helicases as integrators of RNA, nucleotide and protein binding. The multiple functions of RNA helicases as drivers and regulators of gene expression. A novel mechanism for Prp5 function in prespliceosome formation and proofreading the branch site sequence. RNA-methylation-dependent RNA processing controls the speed of the circadian clock. ALKBH5 is a mammalian RNA demethylase that impacts RNA metabolism and mouse fertility. FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis. m6A mRNA methylation facilitates resolution of naïve pluripotency toward differentiation. N(6)-methyladenosine-dependent RNA structural switches regulate RNA-protein interactions. HNRNPA2B1 is a mediator of m(6)A-dependent nuclear RNA processing events. N6-methyladenosine-dependent regulation of messenger RNA stability. N6-methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO. ![]() A METT元-METTL14 complex mediates mammalian nuclear RNA N6-adenosine methylation. Identification of methylated nucleosides in messenger RNA from Novikoff hepatoma cells. Dynamic RNA modifications in posttranscriptional regulation. ![]() mRNA modifications: dynamic regulators of gene expression? RNA Biol. RNA helicase DDX21 coordinates transcription and ribosomal RNA processing. From unwinding to clamping - the DEAD box RNA helicase family. Viral targeting of DEAD box protein 3 reveals its role in TBK1/IKKepsilon-mediated IRF activation. DHX9 pairs with IPS-1 to sense double-stranded RNA in myeloid dendritic cells. Zhang, Z., Yuan, B., Lu, N., Facchinetti, V. The helicase DDX41 recognizes the bacterial secondary messengers cyclic di-GMP and cyclic di-AMP to activate a type I interferon immune response. The helicase DDX41 senses intracellular DNA mediated by the adaptor STING in dendritic cells. Immune signaling by RIG-I-like receptors. Transcriptional repression of IFN regulatory factor 7 by MYC is critical for type I IFN production in human plasmacytoid dendritic cells. Herpesvirus genome recognition induced acetylation of nuclear IFI16 is essential for its cytoplasmic translocation, inflammasome and IFN-b responses. Endogenous TRIM5α function is regulated by SUMOylation and nuclear sequestration for efficient innate sensing in dendritic cells. Siglec1 suppresses antiviral innate immune response by inducing TBK1 degradation via the ubiquitin ligase TRIM27. Self-regulation and cross-regulation of pattern-recognition receptor signalling in health and disease. TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity. Regulation of type I interferon responses. Discriminating self from non-self in nucleic acid sensing. Thus, DDX46 inhibits antiviral innate responses by entrapping selected antiviral transcripts in the nucleus by erasing their m 6A modification, a modification normally required for export from the nucleus and translation. DDX46 also suppressed antiviral innate immunity in vivo. It consequently enforced their retention in the nucleus and therefore prevented their translation and inhibited interferon production. After viral infection, DDX46 recruited ALKBH5, an 'eraser' of the RNA modification N 6-methyladenosine (m 6A), via DDX46's DEAD helicase domain to demethylate those m 6A-modified antiviral transcripts. DDX46 bound Mavs, Traf3 and Traf6 transcripts (which encode signaling molecules involved in antiviral responses) via their conserved CCGGUU element. Here we found that nuclear DDX member DDX46 inhibited the production of type I interferons after viral infection. ![]() Modification of RNA is involved in many biological processes however, its role in antiviral innate immunity has remained unclear. DEAD-box (DDX) helicases are vital for the recognition of RNA and metabolism and are critical for the initiation of antiviral innate immunity.
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