HuD protein has been shown to stabilize mRNAs with AU-rich elements (ARE) in their 3'UTRs, including Gap43 that has been linked to axon growth. HuD also binds to Neuritin (Nrn1), whose 3'UTR contains ARE sequences. Although Nrn1’s 3'UTR was shown to have axonal localizing activity in embryonic hippocampal neurons, it was not active in adult DRG neurons. Here, we asked why the 3'UTR is not sufficient to localize Nrn1 mRNA into DRG axons. HuD overexpression increases the axonal localizing activity of Nrn1’s 3'UTR in DRG. HuD binds directly to Nrn1’s ARE with about two-fold higher affinity than Gap43’s ARE. Though Nrn1 ARE can displace Gap43 ARE from HuD binding, HuD binds to the full 3'UTR of Gap43 with higher affinity such that higher levels of Nrn1 are needed to displace the 3'UTR. Localizing activity of Nrn1’s 3'UTR increases when endogenous Gap43 is depleted from DRG neurons. Taken together, our data indicate that endogenous Nrn1 and Gap43 mRNAs compete for binding to HuD for their axonal localization and activity of Nrn1's 3'UTR.