摘要: The mammalian genome has evolved to encode a battery of mechanisms, mitigate progression in the life cycle an invasive viral pathogen. Although apparently disadvantaged by their dependence on host biosynthetic processes, immensely faster rate evolution provides viruses with edge this conflict. In review, I have discussed potential anti-virus activity Inositol Requiring Enzyme 1 (IRE1), well characterized effector cellular homeostatic response overloading Endoplasmic Reticulum (ER) protein-folding capacity. IRE1, ER-membrane-resident Ribonuclease (RNase), upon activation catalyses regulated cleavage select protein-coding and non-coding RNAs, using RNase domain which is homologous that known anti-viral RNaseL. latter operates as part Oligoadenylate synthetase OAS/RNaseL system defence mechanism. Protein-coding RNA substrates are differentially treated IRE1 either augment, through cytoplasmic splicing intron Xbp1 transcript, or suppress gene expression. This referred suppression expression mediated degradative cohort transcripts, initiating Regulated IRE1-dependent decay RIDD pathway. review first discusses mechanism evasion tactics employed different viruses. followed pathway its effect stability RNAs. conclude comparison enzymatic two RNases deliberations physiological consequences activation.
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