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Updated: Feb 15, 2026

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DAPK1 orchestrates cell division and junction to control corneal epithelial development

Mulin Yang1, Zihe Zhao1, Weiwen Bu2

  • 1Department of Genetics and Cell Biology, College of Life Sciences, Tianjin Key Laboratory of Protein Science, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China.

European Journal of Cell Biology
|February 13, 2026
PubMed

Insights

Death-associated protein kinase 1 (DAPK1) is crucial for healthy corneal development. Its absence causes corneal opacity and abnormal epithelial thickening, highlighting DAPK1 as a therapeutic target for eye diseases.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Developmental Biology

Background:

  • Corneal epithelial stratification is essential for eye protection.
  • The molecular mechanisms governing this process remain incompletely understood.
  • Death-associated protein kinase 1 (DAPK1) is implicated in cellular processes.

Purpose of the Study:

  • To investigate the role of DAPK1 in corneal epithelial development.
  • To elucidate the molecular mechanisms by which DAPK1 influences corneal stratification.
  • To assess the therapeutic potential of DAPK1 in corneal diseases.

Main Methods:

  • Utilized Dapk1 knockout mouse models.
  • Performed immunofluorescence staining with epithelial-specific markers.
  • Analyzed corneal histology and cell junction integrity.

Main Results:

  • DAPK1 is upregulated during corneal epithelial development.
  • DAPK1 deficiency leads to corneal opacity and epithelial thickening.
  • DAPK1 loss disrupts stratification, impairs cell junctions, and causes epidermal-like changes.

Conclusions:

  • DAPK1 plays a critical role in regulating corneal epithelial stratification and development.
  • DAPK1 deficiency results in pathological changes mimicking epidermal development.
  • DAPK1 represents a potential therapeutic target for treating corneal diseases.
Keywords:
Cell divisionCell junctionCorneal epitheliumKnockout mouseStratification

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