Detailed Instructions: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
Problem:Highlights d N 1 -2 0 O-methylation is crucial to block RIG-I activation by viral and self RNA d Self-RNA exclusion is singularly governed by the conserved H830 in RIG-I d H830A alteration leads to indiscriminate recognition of endogenous RNA by RIG-I d Cellular N 1 -2 0 O-methyltransferase knockdown renders endogenous RNA stimulatory SUMMARY The cytosolic helicase retinoic acid-inducible gene-I (RIG-I) initiates immune responses to most RNA viruses by detecting viral 5 0 -triphosphorylated RNA (pppRNA). Although endogenous mRNA is also 5 0 -triphosphorylated, backbone modifications and the 5 0 -ppp-linked methylguanosine ( m7 G) cap prevent immunorecognition. Here we show that the methylation status of endogenous capped mRNA at the 5 0 -terminal nucleotide (N 1 ) was crucial to prevent RIG-I activation. Moreover, we identified a single conserved amino acid (H830) in the RIG-I RNA binding pocket as the mediator of steric exclusion of N 1 -2 0 O-methylated RNA. H830A alteration (RIG-I(H830A)) restored binding of N 1 -2 0 O-methylated pppRNA. Consequently, endogenous mRNA activated the RIG-I(H830A) mutant but not wild-type RIG-I. Similarly, knockdown of the endogenous N 1 -2 0 O-methyltransferase led to considerable RIG-I stimulation in the absence of exogenous stimuli. Studies involving yellow-fever-virus-encoded 2 0 O-methyltransferase and RIG-I(H830A) revealed that viruses exploit this mechanism to escape RIG-I. Our data reveal a new role for cap N 1 -2 0 O-methylation in RIG-I tolerance of self-RNA.
Solution:
A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N 1 -2 0 O-Methylated Self RNA Article A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N 1 -2 0 O-Methylated Self RNA