ArticleResearch (Washington, D.C.)2026
Multi-Omics Analysis Reveals Nono-Kcnq2 Regulation of Neuronal Excitability in Chronic Constriction Injury-Induced Neuropathic Pain.
Article in Research (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
Neuropathic pain, resulting from somatosensory nervous system damage or disease, is a debilitating condition marked by spontaneous pain, hypersensitivity, and sensory abnormalities. Neuropathic pain involves spinal neuronal hyperexcitability, yet its molecular basis remains poorly defined. We utilized a comprehensive multi-omics approach, incorporating proteomics, phosphoproteomics, concatenated tandem array of consensus transcription response elements, and both single-cell and spatial transcriptomics, to chart time-resolved adaptations in the L4 to L6 spinal cord of a chronic constriction injury rat model. Multi-omics revealed remodeling of glutamatergic synapse pathways and identified non-POU (Pit-Oct-Unc) domain-containing octamer binding (Nono) as a down-regulated transcription factor associated with reduced potassium voltage-gated channel subfamily Q member 2 (Kcnq2) expression. Nono and Kcnq2 were co-enriched in neurexin 3-positive and peripherin-positive spinal neurons. Restoring Nono expression up-regulated Kcnq2, enhanced K
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