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Zipper-interacting Protein Kinase Modulates Gene Expression Linked to Synaptic and Neuronal Processes after Traumatic

Yingxue Mei1,2, Lizhen Zheng1, Mengxin He1

  • 1Fujian Key Laboratory of Cognitive Function and Diseases, Institute of Basic Medicine, School of Basic Medical Sciences, Fujian Medical University, 1 Xuefu North Road, Fuzhou, 350122, Fujian, China.

Molecular Neurobiology
|January 12, 2026
PubMed
Summary
This summary is machine-generated.

Zipper-interacting protein kinase (ZIPK) plays a key role in brain gene regulation following traumatic brain injury (TBI). Reducing ZIPK levels helps protect against synaptic damage and may offer a new TBI therapeutic strategy.

Keywords:
Neuronal functionSynaptic functionTranscriptome sequencingTraumatic brain injury (TBI)Zipper-interacting protein kinase (ZIPK)

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Traumatic brain injury (TBI) is a major global cause of death and disability.
  • Zipper-interacting protein kinase (ZIPK) is implicated in neurological disorders, including TBI, and its inhibition can reduce neuronal injury.
  • ZIPK's role in regulating gene expression within the brain after TBI is currently unknown.

Purpose of the Study:

  • To investigate the role of ZIPK in gene expression regulation in the brain following TBI.
  • To identify specific genes and pathways affected by ZIPK in the context of TBI.
  • To explore ZIPK as a potential therapeutic target for TBI.

Main Methods:

  • Transcriptome sequencing to compare gene expression in wild-type and ZIPK heterozygous mice post-TBI.
  • Gene set enrichment analysis to identify key biological pathways.
  • Quantitative real-time PCR, gene correlation, protein-protein interaction analysis, and immunofluorescence staining to validate findings.

Main Results:

  • ZIPK regulates numerous genes and pathways involved in synaptic function, learning, memory, vascular function, and DNA replication after TBI.
  • Gene set enrichment analysis identified a significant role for ZIPK in synaptic regulation during TBI.
  • Validation confirmed ZIPK's influence on synaptic genes (e.g., Drd1, Grin2a, Grin2b, Dlg4, Fn1, Pecam1) and demonstrated that partial ZIPK deletion mitigates TBI-induced synaptic protein loss.

Conclusions:

  • ZIPK is a crucial regulator within the brain's molecular network, particularly concerning synaptic damage following TBI.
  • Targeting ZIPK presents a promising therapeutic avenue for mitigating TBI-related brain injury and dysfunction.