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In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Paragraph: Cells of all mammals recognize double-stranded RNA (dsRNA) as a foreign material. In response, they release interferons (IFNs) and activate a ubiquitously expressed pseudokinase/endoribonuclease RNase L. RNase L executes regulated RNA decay and halts global translation. Here we developed a biosensor for 2',5'oligoadenylate (2-5A), the natural activator of RNase L. We found that 2-5A was acutely synthesized by cells in response to dsRNA sensing, which immediately triggered cellular RNA cleavage by RNase L and arrested host protein synthesis. However, IFNs of types I and III (IFN- and IFN-). Our data suggests that IFNs escape from the action of RNase L on translation. We propose that 2-5A/RNase L pathway serves to rapidly and accurately suppress basal protein synthesis, preserving privileged production of defense proteins of the innate immune system. RNase L is a mammalian enzyme that can stop global protein synthesis during interferon response. Cells must balance the need to make interferons (which are proteins) with the risk to lose cell-wide translation due to RNase L. This balance can most simply be achieved if RNase L was activated late in the interferon response. However, we show by engineering a biosensor for the RNase L pathway, that on the contrary, RNase L activation precedes interferon synthesis. Further, translation of interferons evades the action of RNase L. Our data suggest that RNase L facilitates a switch of protein synthesis from homeostasis to specific needs of innate immune signaling. . CC-BY 4.0 International license is made available under a The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It . https://doi.org/10.1101/476341 doi: bioRxiv preprint The 2-5A system is also a surveillance pathway for endogenous dsRNAs from mammalian genomes. Cells with adenosine deaminase 1 (ADAR1) deficiency accumulate self-dsRNA that promotes 2-5A-driven apoptosis 8 . 2-5A synthesis in the presence of low amounts of endogenous dsRNAs does not cause cell death, but functions as a suppressor of adhesion, proliferation, migration, and prostate cancer metastasis 17,18 . Additionally, activation of the 2-5A system also blocks secretion of milk . CC-BY 4.0 International license is made available under a
Title: Realtime 2-5A kinetics suggests interferons and evade global arrest of translation by RNase L
Output:
False