ArticleiScience2024
DExH-box helicase 9 modulates hippocampal synapses and regulates neuropathic pain.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Sequestration of growth cone surface proteins by cytoplasmic Lrrtm2 inducesbioRxiv : the preprint server for biology · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Comprehensive analysis of circRNA-miRNA-mRNA networks to reveal potential cell death, inflammation and oxidative stress-related targets for postoperative cognitive dysfunction.Frontiers in aging neuroscience · 2026Article
- SERBP1-PCIF1 complex-controlled m6Am modification in glutamatergic neurons of the primary somatosensory cortex is required for neuropathic pain in mice.Nature communications · 2025Article
- mNSF: multi-sample non-negative spatial factorization.Genome biology · 2025Article
- DEAD/DEAH-box RNA helicases shape the risk of neurodevelopmental disorders.Trends in genetics : TIG · 2025Review
- Proteomic analysis of spinal dorsal horn in prior exercise protection against neuropathic pain.Scientific reports · 2025Article
- The role of DEAD- and DExH-box RNA helicases in neurodevelopmental disorders.Frontiers in molecular neuroscience · 2024Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experimental studies have shown that neuropathic pain impairs hippocampal synaptic plasticity. Here, we sought to determine the underlying mechanisms responsible for synaptic changes in neuropathic painful mouse hippocampal neurons. Beyond demonstrating proof-of-concept for the location of DExH-box helicase 9 (DHX9) in the nucleus, we found that it did exist in the cytoplasm and DHX9 depletion resulted in structural and functional changes at synapses in the hippocampus. A decrease of DHX9 was observed in the hippocampus after peripheral nerve injury; overexpression of DHX9 in the hippocampus significantly alleviated the nociceptive responses and improved anxiety behaviors. Mimicking DHX9 decrease evoked spontaneous pain behavioral symptoms and anxiety emotion in naïve mice. Mechanistically, we found that DHX9 bound to
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