A Conserved RNA-binding Protein Contributes to Nociceptive Pain

      This paper is only available as a PDF. To read, Please Download here.
      RNA control permeates neurobiology. Nociceptors are exemplary. Noxious stimuli can induce rapid translation in nociceptors. In prior work, we examined translational efficiency on a genome-wide basis in DRG neurons using ribosome profiling. We found that a single motif was highly enriched in the 3’UTRs of preferentially translated mRNAs. It contains an A/U-rich element bound by HuR. We found that HuR is expressed broadly throughout the PNS. To determine the role of HuR in pain, we made use of a recently described small molecule inhibitor termed CMLD-2. It reduced spontaneous firing of mouse and hiPSC derived sensory neurons. Furthermore, inhibition of HuR in vivo with CMLD-2 blocks hyperalgesic priming and alleviates mechanical hypersensitivity. Elimination of HuR from Nav1.8 expressing neurons ablates hyperalgesic priming. Collectively, this work identifies HuR as a key factor involved in nociceptive plasticity and suggests a new target for pain. Grant support from National Institutes of Health (NIH).
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to The Journal of Pain
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect