ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Palmitoyl Acyltransferase Zdhhc17 Promotes Functional Recovery After Spinal Cord Injury by Targeting the Nuclear Transport Factors Kpna2 and Ipo9.
Meixuan Chen, Huan Chen, Sining Ding, Fan Liu, Xiaofei Zheng, Yuan Wang, Ruitu Tian, Huan Li, Peilin Liu, Le Hu and 3 more
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In one paragraphArticle in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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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13 authors.
Meixuan Chen *Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0009-8176-3950 Huan Chen *Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0000-1676-2630 Sining DingGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Fan LiuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0000-2783-8792 Xiaofei ZhengGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0004-9130-1278 Yuan WangGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Ruitu TianGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Huan LiGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0000-0649-9111 Peilin LiuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Le HuGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-3108-2339 Bin LiuDepartment of Spine Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Mangmang LiGuangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-4182-6509 Funding
Guangdong Provincial Key Laboratory of Bone and Joint Degeneration DiseasesNational Key Research and Development Program of China 2017YFA0105401National Natural Science Foundation of China 82272498
6 · The paper itselfAbstract
In adult mammals, poor functional recovery after spinal cord injury (SCI) is largely due to the very limited capacity to reconstruct damaged neural connections together with neuronal loss. Here, we identify the neuroprotective role of Zdhhc17 as a palmitoyl acyltransferase (PAT) following SCI. Neuron‑specific Zdhhc17 overexpression in vitro and in vivo markedly enhances axon regeneration and functional recovery after SCI in a PAT-activity-dependent manner. Interactome and palmitoylation analyses in cortical neurons identify the karyopherins Kpna2 and Ipo9 as previously unrecognized Zdhhc17 substrates. SCI markedly reduces Kpna2 and Ipo9 protein levels, whereas Zdhhc17‑mediated palmitoylation stabilizes them by suppressing their ubiquitin‑dependent degradation. Functionally, neuronal overexpression of Kpna2 or Ipo9 mimics the therapeutic effects of Zdhhc17, and co‑expression of Zdhhc17 with Ipo9, but not Kpna2, further augments SCI repair. Using H
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axoncell biologyexcitotoxicityinteractomeneuroprotectionoxidative stresspalmitoylationprotein palmitoylationspinal cord injury
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PMID42725791
PMCPMC13564187
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