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According to the prevailing m6A reader model, YTHDF1 functions to promote mRNA translation by recruiting various translation factors, such as eIF3, to marked mRNAs (95, 98)

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Pharmacological studies have demonstrated that PPAR- agonists are efficacious in rodent models of inflammatory and autoimmune diseases, and a neuropathic pain model in which the PPAR- has been genetically deleted showed a loss of PEA effectiveness, thus suggesting that PEA may act as PPAR- agonist [24]