ArticleCNS neuroscience & therapeutics2022
SUMOylation of Kir7.1 participates in neuropathic pain through regulating its membrane expression in spinal cord neurons.
Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- SUMO Regulation of Ion Channels in Health and Disease.Physiology (Bethesda, Md.) · 2025Review
- SUMOylation and DeSUMOylation: Tug of War of Pain Signaling.Molecular neurobiology · 2025Review
- Exploring Ubiquitination in Spinal Cord Injury Therapy: Multifaceted Targets and Promising Strategies.Neurochemical research · 2025Review
- Spinal neuron-glial crosstalk and ion channel dysregulation in diabetic neuropathic pain.Frontiers in immunology · 2025Review
- Crosstalk between PKA and PIAS3 regulates cardiac Kv4 channel SUMOylation.Cell communication and signaling : CCS · 2024Article
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- Downregulation of ciRNA-Kat6b in dorsal spinal horn is required for neuropathic pain by regulating Kcnk1 in miRNA-26a-dependent manner.CNS neuroscience & therapeutics · 2023Article
- SUMOylation of Kir7.1 participates in neuropathic pain through regulating its membrane expression in spinal cord neurons.CNS neuroscience & therapeutics · 2022Article
- Ion-channel mRNA expression alterations in a cervical dorsal horn compression induced novel rabbit model of trigeminal neuropathic pain.Science progressArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPotassium (K METHODS AND
resultsNeuropathic pain was induced by spared nerve injury (SNI). The mechanical sensitivity was assessed by von Frey test. Immunofluorescence staining assay revealed that Kir7.1 was predominantly expressed in spinal neurons but not astrocytes or microglia in normal rats. Western blot results showed that SNI markedly decreased the total and membrane expression of Kir7.1 in the spinal dorsal horn accompanied by mechanical hypersensitivity. Blocking Kir7.1 with the specific antagonist ML418 or knockdown kir7.1 by siRNA led to mechanical allodynia. Co-IP results showed that the spinal kir7.1 channels were decorated by SUMO-1 but not SUMO-2/3, and Kir7.1 SUMOylation was upregulated following SNI. Moreover, inhibited SUMOylation by GA (E1 inhibitor) or 2-D08 (UBC9 inhibitor) can increase the spinal surface Kir7.1 expression.
conclusionSUMOylation of the Kir7.1 in the spinal cord might contribute to the development of SNI-induced mechanical allodynia by decreasing the Kir7.1 surface expression in rats.
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