ArticleNature communications2018
Inhibition of Poly(A)-binding protein with a synthetic RNA mimic reduces pain sensitization in mice.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 179 citations in OpenAlex.
- Article
- Efficient genetic perturbation of murine sensory neurons in vivo using CRISPR/Cas9.The journal of pain · 2026Article
- Hydrogel microspheres loaded with sinomenine and Drynaria rhizome enhance the treatment of rheumatoid arthritis via immune regulation and promoting bone repair.Journal of nanobiotechnology · 2026Article
- Article
- GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025Article
- Efficient genetic perturbation of murine sensory neuronsbioRxiv : the preprint server for biology · 2025Article
- The mRNA Translation Inhibitor Vioprolide A Prevents Inflammatory Pain-Like Behaviour With Limited Action on Already Established Pain-Like Behaviour in Mice.European journal of pain (London, England) · 2025Article
- Voltage-Gated Calcium Channels Play a Central Role in Caenorhabditis elegans Response to Noxious Heat.Neurochemical research · 2025Article
- Article
- A nociceptor-specific RNAi screen inPeerJ · 2025Article
- Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024Article
- Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.bioRxiv : the preprint server for biology · 2024Article
- Regulation of rheumatoid arthritis microenvironmentBioactive materials · 2024Article
- An engineered poly(A) tail attenuates gut ischemia/reperfusion-induced acute lung injury.Surgery · 2024Article
- A Synthetic Poly(A) Tail Targeting Extracellular CIRP Inhibits Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Discovery and mechanism-guided engineering of BHET hydrolases for improved PET recycling and upcycling.Nature communications · 2023Article
- Inhibition of Nonsense-Mediated Decay Induces Nociceptive Sensitization through Activation of the Integrated Stress Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- An engineered miRNA PS-OMe miR130 inhibits acute lung injury by targeting eCIRP in sepsis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Dual Leucine Zipper Kinase Regulates Dscam Expression through a Noncanonical Function of the Cytoplasmic Poly(A)-Binding Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Chemically Modified Poly(A) Analogs Targeting PABP: Structure Activity Relationship and Translation Inhibitory Properties.Chemistry (Weinheim an der Bergstrasse, Germany) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nociceptors rely on cap-dependent translation to rapidly induce protein synthesis in response to pro-inflammatory signals. Comparatively little is known regarding the role of the regulatory factors bound to the 3' end of mRNA in nociceptor sensitization. Poly(A)-binding protein (PABP) stimulates translation initiation by bridging the Poly(A) tail to the eukaryotic initiation factor 4F complex associated with the mRNA cap. Here, we use unbiased assessment of PABP binding specificity to generate a chemically modified RNA-based competitive inhibitor of PABP. The resulting RNA mimic, which we designated as the Poly(A) SPOT-ON, is more stable than unmodified RNA and binds PABP with high affinity and selectivity in vitro. We show that injection of the Poly(A) SPOT-ON at the site of an injury can attenuate behavioral response to pain. Collectively, these results suggest that PABP is integral for nociceptive plasticity. The general strategy described here provides a broad new source of mechanism-based inhibitors for RNA-binding proteins and is applicable for in vivo studies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.